"Essential" Hypertension And Appreciating It For What It Really Is

[Tristan Loscha]

I am almost at wit's end in bring down my high blood pressure levels. Lately, instead of it going down, it has gone higher - thanks to my tireless efforts!

The last reading I got today was 213/138, which is a lot worse than when I stabilized at 180/120 over a year ago. This is already after I had the original cause of my high blood pressure eliminated last year - periodontal infection. Perhaps I would be better off letting things be after that event. But no, I had to try using proteolytic enzymes to lyse the capillary (and arterial) plaque, to clear the piping, so to speak. Little did I know that this would trigger both bacteria and endotoxins to be released, as they are let loose from the plaque.

Observing CBC blood tests, I could see my WBC go up, indicating an increased immune response, with the neutrophil count going up because of the increased bacterial presence in blood, as well as increased monocyte, which I believe to be associated with increased macrophage activity in dealing with endotoxins. As I look back to my CBC records of 2002, when I last had regular blood pressure of 120/80, I realized that my monocyte was at a low value of 3.0, which was less than half of my current monocyte, at 6.7.

It is on this basis that I believe that it is the endotoxins in my system that is the chief cause of my high blood pressure. Monocytes turn into macrophages, and macrophages are involved in the TLR4 inflammatory response to endotoxins. As long as the TLR4 response is active, my monocytes will remain high. With this inflammatory response present, needed substates such as NADPH for producing nitric oxide as a vasodilator will be diverted, and this would be a cause for high blood pressure.

Another cause of high blood pressure is the low level of albumin in my blood. At 42, it is about 5 points lower than the value when my blood pressure was normal, at 47. Albumin attracts sodium ions, and with less albumin, less sodium ions are attracted to form plasma. With less sodium in the plasma, less water can be attracted by osmosis from the ecf into plasma. With less plasma, there is less blood volume. With less blood volume, blood pressure would have to increase to compensate for the lower blood volume.

Albumin is low because albumin is being used to bind with endotoxin into a complex, which would allow endotoxin to be safely excreted through urinary and fecal routes.

Given that the use of proteolytic enzymes to lyse plaque causes more endotoxins to be released, I was considering stopping altogether the use of proteolytic enzymes. But since the enzymes are needed to lyse plaque (as well as immune complexes, formed from antibodies and antigens), I cannot dispense with the use of such enzymes. I would have to either cycle the use of these enzymes, or use them at a lower dosage, such that I can continue to unblock the glomerular capillaries in my kidneys. The kidneys is where my hypertension originates. This is evidenced by my high serum creatinine, establishing that I have lower glomerular filtration rates, a sign of poor kidney condition, and the kidney's condition of microalbuminuria, where the kidneys are allowing albumin to pass through, which it shouldn't be doing

I now have to find a way also to manage the endotoxins in the blood such that: 1) it gets excreted out with a rapid transit time, and 2)the TLR4 inflammatory response is controlled and minimized.

So, in summary, I would continue to lyse kidney glomerular capillary plaque, albeit at a reduced rate (in order to control the rate of endotoxin release from lysed plaque) and then to avail of the use of substances that would control the inflammatory TLR4 response.

to be continued...

Good thinking.my current understanding is that sodium through: SGK1-IL23-TH17-IL17 cascade drives an autoimmune
reaction to the entire field that is receptive to the changed cytokine environment driven by sodium-retention.
my advice would be 1-3g NaCl per day.500-1000mg sodium is the physiologic amount,and my hunch is that you are good
at salt-retention,salt-sensitive.we are on the ray peat forums,and peat is a salt-fan,so there is possibility if you followed
his advice you are salted up to the gills already.My understanding.The Renin-aldosterone-Angiotensine System
doesnt really matter,it is an autoimmune disease triggered and maintained by high sodium-tonicity.after a couple of months inflammation will be reduced,(lipid peroxidation cut in half after a week already )also better potassium balance without necessity to increase amount,after 500 to 1000mg
sodium per day,potassium excretion increases 3to4-fold.i would also advise against potassium bicarbonate because of moderate lead-zinc-iron impurities.

 

[Tristan Loscha]

You try a low-VA diet?

I'm 34 and have been a stage 2 hypertensive for the past 5 years, has not responded to anything I've tried in the past like fasting, exercise, low-fat, Bueteyko, etc.. 5 months ago my blood pressure reached a high of 200/95. After 10 weeks of low-VA diet it was down to 130/80. I since stopped doing low-VA and am back to consuming close to RDI levels for the past couple months, but my blood pressure is still down. I also started eating much more saturated fat about 2 weeks ago, don't know if this has played any role but saturated fat supposedly helps over time with lowering endotoxin.

Also this.I dont believe in Poison A talk at all,but Genereux is clean-eating.im not hypertensive but becoming if i have
bad reaction to food.

 

[Tristan Loscha]

The pathogenesis of left ventricular hypertrophy in patients with CKD is incompletely understood. Sodium
intake, which is usually assessed by measuring urinary sodium excretion, has been inconsistently linked
with left ventricular hypertrophy. However, tissues such as skin and muscle may store sodium.






ABSTRACT
The pathogenesis of left ventricular hypertrophy in patients with CKD is incompletely understood. Sodium
intake, which is usually assessed by measuring urinary sodium excretion, has been inconsistently linked
with left ventricular hypertrophy. However, tissues such as skin and muscle may store sodium. Using
23
sodium-magnetic resonance imaging, a technique recently developed for the assessment of tissue so-
dium content in humans, we determined skin sodium content at the level of the calf in 99 patients with mild
to moderate CKD (42 women; median [range] age, 65 [23
–
78] years). We also assessed total body over-
hydration (bioimpedance spectroscopy), 24-hour BP, and left ventricular mass (cardiac magnetic reso-
nance imaging). Skin sodi
um content, but not total body overhydr
ation, correlated
with systolic BP
(
r
=0.33,
P
=0.002). Moreover, skin sodium content correlated more strongly than total body overhydration
did with left ventricular mass (
r
=0.56,
P
,
0.001 versus
r
=0.35,
P
,
0.001;
P
,
0.01 between the two corre-
lations). Linear regression analysis demonstrated that skin sodium content is a strong explanatory variable
for left ventricular mass, unaffected by BP and total body overhydration. In conclusion, we found skin
sodium content to be closely linked to left ventricular mass in patients with CKD. Interventions that reduce
skin sodium content might improve cardiovascular outcomes in these patients.

 

[Tristan Loscha]

https://opus4.kobv.de/opus4-fau/frontdoor/deliver/index/docId/3137/file/bpu2008026001095.pdf



Abstract
Electrolyte and body fluid homeostasis in higher vertebrates
is believed to be fully understood. The paradigm is that Na +
is restricted mainly to the extracellular fluid and K + to the intracellular
space, where both ions act to hold water and
thereby control the extracellular and intracellular fluid volume
by their osmotic activity. Na + accumulation thus inevitably
leads to water retention. The constancy of the extracellular
volume is the task of the kidneys, which control the
total body Na + content. More recent data from balance studies
in humans have questioned this traditional view, suggesting
that large amounts of Na + can be accumulated without
accompanying water retention by osmotically inactive
Na + retention, or by osmotically neutral Na + /K + exchange.
Besides the control of the body Na + content by the kidneys,
redistribution of body electrolytes hence provides an extrarenal
regulatory alternative in the maintenance of body fluid
volume and blood pressure control.



Startling Data from Long-Term Balance Studies in
Humans: Na + Accumulation May Not Lead to Volume
Retention


Where Is the Salt?


Water-Free Na + Retention in Experimental Models of
Salt-Sensitive Hypertension


Deoxycorticosterone
acetate (DOCA) treatment, a favorite
animal model of mineralocorticoid-induced salt-sensitive
hypertension, led to Na + excess in rats, increasing
their total body Na + content by 40–50% within 5 weeks
[14] , but only ; 20% of the Na + accumulated led to volume
retention, leading to only moderate increases in the
total body water content despite massive Na + retention.




Whether local hyperosmolality in osmotically
inactive extracellular Na + reservoirs links dietary
NaCl excess with chronic extracellular inflammation
[17] is currently under investigation. Furthermore,
whether water-free Na + retention to maintain volume homeostasis
in states of body Na + excess decreases blood
pressure by its ‘volume-buffering’ effect, or increases
blood pressure by redistribution of cellular Na + and K +
which may modulate vascular tone, remains to be investigated.

 

[yerrag]

@Tristan Loscha Yes, salt would be helpful. Only problem is that it's not helping build blood volume in my situation. I think it's because my serum albumin can't increase due to it being used to bind endotoxin for excretion. Have to deal first with exhausting my body of its endotoxin stores.

And yes, potassium salts contain impurities. Better to get potassium through food sources.

 

[Terma]

I started using carnitine fumarate again because I was impressed at some of its documented effects and I seem to need some now, force of things, and I am betting on it being more beneficial than harmful in such condition. I figure fatty acid and propionic acid buildup are probably involved in my cells/issues along with immune regulation, Nrf2 and PPAR, and it is quite involved in handling all of them. This review mentions its use in hypertension (L-NAME) several times and I figure you might be interested:
http://www.feedfood.co.uk/download/Carnitine_Enigma_2.pdf
https://www.researchgate.net/publication/281279882_Antioxidant_Action_of_Carnitine_Molecular_Mechanisms_and_Practical_Applications
No point quoting because it is super dense, see "Carnitine and Nrf2 regulation"/"Carnitine and NF-κB regulation"/"Carnitine and PPARs regulation".

I also found this review on NO fairly good to complete any missing knowledge:
Nitric oxide synthases: regulation and function
That's about all I had time to read (prioritizing has become difficult) but it happens to be up your alley although it's unlikely we have same issues. Cheers

 

[yerrag]

I started using carnitine fumarate again because I was impressed at some of its documented effects and I seem to need some now, force of things, and I am betting on it being more beneficial than harmful in such condition. I figure fatty acid and propionic acid buildup are probably involved in my cells/issues along with immune regulation, Nrf2 and PPAR, and it is quite involved in handling all of them. This review mentions its use in hypertension (L-NAME) several times and I figure you might be interested:
http://www.feedfood.co.uk/download/Carnitine_Enigma_2.pdf
https://www.researchgate.net/publication/281279882_Antioxidant_Action_of_Carnitine_Molecular_Mechanisms_and_Practical_Applications
No point quoting because it is super dense, see "Carnitine and Nrf2 regulation"/"Carnitine and NF-κB regulation"/"Carnitine and PPARs regulation".

I also found this review on NO fairly good to complete any missing knowledge:
Nitric oxide synthases: regulation and function
That's about all I had time to read (prioritizing has become difficult) but it happens to be up your alley although it's unlikely we have same issues. Cheers

Thanks for the links. It'll come in handy as I continue to figure out my condition.

 

[yerrag]

I am almost at wit's end in bring down my high blood pressure levels. Lately, instead of it going down, it has gone higher - thanks to my tireless efforts!

The last reading I got today was 213/138, which is a lot worse than when I stabilized at 180/120 over a year ago. This is already after I had the original cause of my high blood pressure eliminated last year - periodontal infection. Perhaps I would be better off letting things be after that event. But no, I had to try using proteolytic enzymes to lyse the capillary (and arterial) plaque, to clear the piping, so to speak. Little did I know that this would trigger both bacteria and endotoxins to be released, as they are let loose from the plaque.

Observing CBC blood tests, I could see my WBC go up, indicating an increased immune response, with the neutrophil count going up because of the increased bacterial presence in blood, as well as increased monocyte, which I believe to be associated with increased macrophage activity in dealing with endotoxins. As I look back to my CBC records of 2002, when I last had regular blood pressure of 120/80, I realized that my monocyte was at a low value of 3.0, which was less than half of my current monocyte, at 6.7.

It is on this basis that I believe that it is the endotoxins in my system that is the chief cause of my high blood pressure. Monocytes turn into macrophages, and macrophages are involved in the TLR4 inflammatory response to endotoxins. As long as the TLR4 response is active, my monocytes will remain high. With this inflammatory response present, needed substates such as NADPH for producing nitric oxide as a vasodilator will be diverted, and this would be a cause for high blood pressure.

Another cause of high blood pressure is the low level of albumin in my blood. At 42, it is about 5 points lower than the value when my blood pressure was normal, at 47. Albumin attracts sodium ions, and with less albumin, less sodium ions are attracted to form plasma. With less sodium in the plasma, less water can be attracted by osmosis from the ecf into plasma. With less plasma, there is less blood volume. With less blood volume, blood pressure would have to increase to compensate for the lower blood volume.

Albumin is low because albumin is being used to bind with endotoxin into a complex, which would allow endotoxin to be safely excreted through urinary and fecal routes.

Given that the use of proteolytic enzymes to lyse plaque causes more endotoxins to be released, I was considering stopping altogether the use of proteolytic enzymes. But since the enzymes are needed to lyse plaque (as well as immune complexes, formed from antibodies and antigens), I cannot dispense with the use of such enzymes. I would have to either cycle the use of these enzymes, or use them at a lower dosage, such that I can continue to unblock the glomerular capillaries in my kidneys. The kidneys is where my hypertension originates. This is evidenced by my high serum creatinine, establishing that I have lower glomerular filtration rates, a sign of poor kidney condition, and the kidney's condition of microalbuminuria, where the kidneys are allowing albumin to pass through, which it shouldn't be doing

I now have to find a way also to manage the endotoxins in the blood such that: 1) it gets excreted out with a rapid transit time, and 2)the TLR4 inflammatory response is controlled and minimized.

So, in summary, I would continue to lyse kidney glomerular capillary plaque, albeit at a reduced rate (in order to control the rate of endotoxin release from lysed plaque) and then to avail of the use of substances that would control the inflammatory TLR4 response.

to be continued...

Very high blood pressure continues to plague me.

At a recent blood test, my serum creatinine shot way up to 1.47 mg/dl, much higher than that taken last February, at 1.16. This puts me into chronic kidney disease territory, as this is way above the optimal range of 0.8 - 1.1 (based on Dr. Weatherby). Given that this was a recent occurrence, and very likely linked to increased endotoxin exposure as of late, this could be something I could recover from. It's evident that my recent foray into using proteolytic enzymes backfired, as it caused a lot of endotoxins to be released from lysed plaque, and my high serum creatinine is but one example of how my body has been negatively affected.

My RBC jumped from 5.28 to 5.71, Hemoglobin from 154 to 168, and Hematocrit from 0.45 to 0.48, compared to 2 months ago; my low blood volume grew even worse. This is indicative of low serum albumin that got worse. While my serum albumin would appear to be unchanged, compared to 5 months ago, from 4.19 to 4.27 g/L, I have to take into account that in terms of total albumin, my serum albumin has gone down because the blood volume has gone down. Since total serum albumin plays a huge role in determining the blood volume, low total serum albumin would cause blood pressure to go up, as lower blood volume (from lower serum albumin) causes higher blood pressure to compensate for it.

The heavy endotoxin load I experienced from its release from the lysing of plaque is that it requires the use of albumin to bind to it, and I believe that it is the reason why I urinated so much, as it is thru urine that the endotoxin bound to albumin is excreted. The excessive urination has caused my serum albumin to go down, and with this my blood volume has gone down as well. And with that, my blood pressure would be increased to compensate for the lower blood volume.

I'm not sure how much my liver has been impacted by the endotoxin load, as my SGPT has increased from 30 to 37.2, while my SGOT has decreased from 30 to 26.40, with a value of 30 and higher being a negative. I'm slightly concerned as a high endotoxin load could put a great load on the liver, and the liver may be overwhelmed that it won't do a good job at detoxifying toxins and excess hormones. If say, estrogen gets past the liver, it could cause some biliary dysfunction.

But there is a silver lining to this though. Serum uric acid has gone down from 383 to 364 umol/L (from 11 months ago). And RDW (red blood cell distribution width) has gone down from 13.7 to 13.1 (from 2 months ago). This could mean that the lysing of plaque is working. Perhaps there is less oxidative stress, as indicated by lower uric acid, and less restriction in the capillaries, as indicated by lower RDW.

It's too early to draw definite conclusions, but it's giving me a glimmer of hope that not all is lost. The increased blood pressure and the increased creatinine would normally get me worried, but I believe that increasing blood volume would not be a difficult task moving forward. I would have to increase my serum albumin for now before taking any more proteolytic enzymes. I'll have to eat more protein to increase albumin production, and I'll also have to increase intake of electrolytes. Once my blood volume goes back to normal, I can expect to see lower blood pressure.

Further down the line, I see myself exploring the use of Chinese herbs. I have ordered an Chinese herbal blend from a US source. I hope I have a good supplier in Activeherbs. I don't trust the herbal blends I could find in the Philippines. I need to make sure the herbal blends I get are of the potency they claim they are, and that they're free from heavy metals. Nothing could be as bad as getting medicine that makes your worse off.

I think I've pretty much found the cause of my hypertension, and that's already half the battle. I'm now left to find the right protocol to eliminate the cause. It would be nice if I could remove plaque with no endotoxin side-effects, but since that isn't the case, I'll have to find a right method to do lyse plaque while being able to deal with the endotoxin side effects. Perhaps this will involve some sort of cycling. We shall see.

 

[Tristan Loscha]

Very high blood pressure continues to plague me.

At a recent blood test, my serum creatinine shot way up to 1.47 mg/dl, much higher than that taken last February, at 1.16. This puts me into chronic kidney disease territory, as this is way above the optimal range of 0.8 - 1.1 (based on Dr. Weatherby). Given that this was a recent occurrence, and very likely linked to increased endotoxin exposure as of late, this could be something I could recover from. It's evident that my recent foray into using proteolytic enzymes backfired, as it caused a lot of endotoxins to be released from lysed plaque, and my high serum creatinine is but one example of how my body has been negatively affected.

My RBC jumped from 5.28 to 5.71, Hemoglobin from 154 to 168, and Hematocrit from 0.45 to 0.48, compared to 2 months ago; my low blood volume grew even worse. This is indicative of low serum albumin that got worse. While my serum albumin would appear to be unchanged, compared to 5 months ago, from 4.19 to 4.27 g/L, I have to take into account that in terms of total albumin, my serum albumin has gone down because the blood volume has gone down. Since total serum albumin plays a huge role in determining the blood volume, low total serum albumin would cause blood pressure to go up, as lower blood volume (from lower serum albumin) causes higher blood pressure to compensate for it.

The heavy endotoxin load I experienced from its release from the lysing of plaque is that it requires the use of albumin to bind to it, and I believe that it is the reason why I urinated so much, as it is thru urine that the endotoxin bound to albumin is excreted. The excessive urination has caused my serum albumin to go down, and with this my blood volume has gone down as well. And with that, my blood pressure would be increased to compensate for the lower blood volume.

I'm not sure how much my liver has been impacted by the endotoxin load, as my SGPT has increased from 30 to 37.2, while my SGOT has decreased from 30 to 26.40, with a value of 30 and higher being a negative. I'm slightly concerned as a high endotoxin load could put a great load on the liver, and the liver may be overwhelmed that it won't do a good job at detoxifying toxins and excess hormones. If say, estrogen gets past the liver, it could cause some biliary dysfunction.

But there is a silver lining to this though. Serum uric acid has gone down from 383 to 364 umol/L (from 11 months ago). And RDW (red blood cell distribution width) has gone down from 13.7 to 13.1 (from 2 months ago). This could mean that the lysing of plaque is working. Perhaps there is less oxidative stress, as indicated by lower uric acid, and less restriction in the capillaries, as indicated by lower RDW.

It's too early to draw definite conclusions, but it's giving me a glimmer of hope that not all is lost. The increased blood pressure and the increased creatinine would normally get me worried, but I believe that increasing blood volume would not be a difficult task moving forward. I would have to increase my serum albumin for now before taking any more proteolytic enzymes. I'll have to eat more protein to increase albumin production, and I'll also have to increase intake of electrolytes. Once my blood volume goes back to normal, I can expect to see lower blood pressure.

Further down the line, I see myself exploring the use of Chinese herbs. I have ordered an Chinese herbal blend from a US source. I hope I have a good supplier in Activeherbs. I don't trust the herbal blends I could find in the Philippines. I need to make sure the herbal blends I get are of the potency they claim they are, and that they're free from heavy metals. Nothing could be as bad as getting medicine that makes your worse off.

I think I've pretty much found the cause of my hypertension, and that's already half the battle. I'm now left to find the right protocol to eliminate the cause. It would be nice if I could remove plaque with no endotoxin side-effects, but since that isn't the case, I'll have to find a right method to do lyse plaque while being able to deal with the endotoxin side effects. Perhaps this will involve some sort of cycling. We shall see.

There are some indications that your condition is Salt-Sensitive Hypertension,It is caused by "osmotically neutral Sodiumretention".The
condition Hypertension,peat confuses Blood-Pressure-Points
with the actual disease-state Hypertension.(It isnt just more bloodpressure points.It is a distinct syndrome,vascular inflammation of an autoimmune type.)All these renal signs also,what are they doing when kidney disease was initated?
Low-Salt-Diet, LSD.
Salt is directly kidney-toxic, the upconcentration of acidic Salt-Urine acid-damages the renal system,you get metabolic acidosis from renal-physiologic handling of the excessive Chlorine by deranged elimination of Bicarbonate.
I would advise for an intake of no more than 1 to 3 grams of NaCl from all sources,no more artifical saltsupplement from
the dispenser.Natural occuring Salt,meat has 600mg Na per KILO.

 

[yerrag]

There are some indications that your condition is Salt-Sensitive Hypertension,It is caused by "osmotically neutral Sodiumretention".The
condition Hypertension,peat confuses Blood-Pressure-Points
with the actual disease-state Hypertension.(It isnt just more bloodpressure points.It is a distinct syndrome,vascular inflammation of an autoimmune type.)All these renal signs also,what are they doing when kidney disease was initated?
Low-Salt-Diet, LSD.
Salt is directly kidney-toxic, the upconcentration of acidic Salt-Urine acid-damages the renal system,you get metabolic acidosis from renal-physiologic handling of the excessive Chlorine by deranged elimination of Bicarbonate.
I would advise for an intake of no more than 1 to 3 grams of NaCl from all sources,no more artifical saltsupplement from
the dispenser.Natural occuring Salt,meat has 600mg Na per KILO.

Thanks, but I'm not convinced with your argument. Since salt is needed to increase osmolarity in order to attract water from the ecf into plasma, it makes no sense to restrict salt intake.

That being said, it's important that there is enough albumin to be able to attract enough salt around it in order to build blood volume. With low albumin, increased salt intake is useless.

Then there is the matter of balance. If I'm deficient in potassium, it would also be counterproductive increasing salt intake. And if I wanted to increase my potassium stores, I would. need to make sure I have good magnesium stores.

You could be right that salt can cause increased blood pressure, from a standpoint of low magnesium and potassium stores.

 

[Tristan Loscha]

..too high total bodywater?
whats your weight,height approx bodyfatmass,etc

It isnt about Fluid dynamics in hypertension in my opinion,although in general Blood-Pressure Point measure it is.But Hypertension is not higher Bloodpressure moving along a line until it is too high,it is symptomatology of whole body inflammation,with hypertension as a biological sign on top,signifying.
it is a inflammtory condition.
It decreases eNOS and Arginase,something like Viagra is doing it more locally diametrically.


Either you have too much fluid in the active circulation,or weigh down and compression of your venous system through physical weight and concomitant tissue compression,Or vascular reduction in circumference by the Anti-Viagra-Effect
of NaCl,by virtue of induction of Th17-Inflammation,which reduces needed(no one says CO2 please!)eNOS-
availability,thus lowering needed local NO,delivered to us by eNOS.


Also,you have accrued an large amount of sodium already,so it takes a couple of months to come off of excess.
Humans are highly,highly competent to retain Sodium,Peat didnt read or understood the World-Literature in that
regard.
Maybe he is inferring from his own experience,but the literature is ruled by different thought.Maybe they are right,?

I read a lot of Observations and Experiences of actual Hands-On clinicians and active researchers.
We are taking Supraphysiologic amount of NaCl in,and all we have to show for it is stale Angiotensin and Aldosterone-
hydraulics.Salt Loading is over.

 

[Tristan Loscha]

..


Microvascular structure and function in salt-sensitive hypertension.
Review article
Boegehold MA. Microcirculation. 2002.
Show full citation
Abstract

In many individuals with essential hypertension, dietary salt can further increase blood pressure by augmentation of an already elevated total peripheral resistance. There is little information on the microvascular changes that contribute to salt-sensitive hypertension in humans, but studies in the Dahl salt-sensitive rat have provided some knowledge of the microcirculation in this form of hypertension. These studies, most of which have used intravital microscopy or isolated vessel technology, are the focus of this review. The salt-induced exacerbation of hypertension in Dahl rats is due to a uniform increase in hemodynamic resistance throughout most of the peripheral vasculature. In the spinotrapezius muscle, this resistance increase is largely due to the intense constriction of proximal arterioles. The mechanisms responsible for this increased arteriolar tone include increased responsiveness to oxygen and a loss of tonic nitric oxide (NO) availability caused by reduced endothelial NO production and/or accelerated NO degradation by reactive oxygen species. Within the last decade, it has become increasingly clear that high salt intake can also lead to changes in microvascular structure and function in the absence of increased arterial pressure. This effect must also be considered when evaluating microvascular changes and their functional consequences in salt-sensitive hypertension.



High salt intake reduces endothelium-dependent dilation of mouse arterioles via superoxide anion generated from nitric oxide synthase.
Nurkiewicz TR, et al. Am J Physiol Regul Integr Comp Physiol. 2007.
Authors
Nurkiewicz TR1, Boegehold MA.
Author information

1
Center for Interdisciplinary Research in Cardiovascular Sciences, West Virginia University School of Medicine, PO Box 9105, Robert C. Byrd Health Sciences Center, Morgantown, WV 26506-9105, USA.

Citation

Am J Physiol Regul Integr Comp Physiol. 2007 Apr;292(4):R1550-6. Epub 2006 Nov 30.
Abstract

In skeletal muscle arterioles of normotensive rats fed a high salt diet, the bioavailability of endothelium-derived nitric oxide (NO) is reduced by superoxide anion. Because the impact of dietary salt on resistance vessels in other species is largely unknown, we investigated endothelium-dependent dilation and oxidant activity in spinotrapezius muscle arterioles of C57BL/6J mice fed normal (0.45%, NS) or high salt (7%, HS) diets for 4 wk. Mean arterial pressure in HS mice was not different from that in NS mice, but the magnitude of arteriolar dilation in response to different levels of ACh was 42-57% smaller in HS mice than in NS mice. Inhibition of nitric oxide synthase (NOS) with N(G) monomethyl L-arginine (L-NMMA) significantly reduced resting diameters and reduced responses to ACh (by 45-63%) in NS mice but not in HS mice. Arteriolar wall oxidant activity, as assessed by tetranitroblue tetrazolium reduction or hydroethidine oxidation, was greater in HS mice than in NS mice. Exposure to the superoxide scavenger 2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPO) + catalase reduced this oxidant activity to normal and restored normal arteriolar responsiveness to ACh in HS mice but had no effect in NS mice. L-NMMA also restored arteriolar oxidant activity to normal in HS mice. ACh further increased arteriolar oxidant activity in HS mice but not in NS mice, and this effect was prevented with L-NMMA. These data suggest that a high salt diet promotes increased generation of superoxide anion from NOS in the murine skeletal muscle microcirculation, thus impairing endothelium-dependent dilation through reduced NO bioavailability.




Reduced arteriolar responses to skeletal muscle contraction after ingestion of a high salt diet.
Marvar PJ, et al. J Vasc Res. 2005 May-Jun.
Show full citation
Abstract

We previously reported that in skeletal muscle arterioles of rats fed a very high salt (HS; 7%) diet, the bioavailability of endothelium-derived nitric oxide (NO) is reduced through scavenging by reactive oxygen species. Because arteriolar NO can play an important role in local blood flow control, we investigated whether arteriolar responses to increased tissue metabolism become compromised in skeletal muscle of salt-fed rats. Consumption of a HS (4%) diet for 4 weeks had no effect on arteriolar diameters, volume flow or shear stress in resting spinotrapezius muscle. Arteriolar responses to a modest elevation in metabolic demand (0.5 Hz contraction) were not different from those in rats fed a normal diet, but diameter responses to a greater elevation in metabolic demand (4 Hz contraction) were significantly less in HS rats than in rats fed a normal diet. In both groups, the NO synthase inhibitor N(G)-monomethyl-L-arginine reduced resting arteriolar diameters and flow by a similar amount and had little or no effect on arteriolar diameter or flow responses to muscle contraction. Arterioles in HS rats exhibited an increase in overall oxidant activity (tetranitroblue tetrazolium reduction) but not in superoxide activity (dihydroethidine oxidation). Reactive oxygen species scavengers (2,2,6,6-tetramethylpiperidine-N-oxyl and catalase) did not normalize the reduced arteriolar responses to muscle contraction in HS rats. These findings suggest that increased oxidant activity in the arteriolar network of salt-fed rats is not due to accumulation of superoxide anion and that neither this oxidant activity nor reduced NO availability can account for the blunted active arteriolar dilation in rats fed a 4% salt diet.



They arent sure of the mechanisms,but they do know that it increases pressure,for Salt-Sensitive Individuals even moreso.

 

[Amazoniac]

@yerrag, what was the reason for poor oral health?

Have you tried to use the proteolytic enzymes away from vitamin C? This is the opposite of the initial idea. I was wondering if it could free up iron or copper somehow. If I'm not wrong, it takes about 12 hours after C dosing for it to return to (circulation) baseline.
What's your experience with food-based vitamin C?

And the longer-chain menaquinones?

 

[yerrag]

hat was the reason for poor oral health?

I wasn't going regularly to the dentist for oral prophylaxis. I was just brushing my teeth and flossing regularly. It wasn't enough as plaque forms easily on my teeth. My teeth probably leeches also, due to poor calcium intake. So my dental enamel wasn't a particularly strong barrier to endotoxins penetrating into teeth around the gumline, and endotoxins could easily be followed by infection.

Have you tried to use the proteolytic enzymes away from vitamin C? This is the opposite of the initial idea. I was wondering if it could free up iron or copper somehow. If I'm not wrong, it takes about 12 hours after C dosing for it to return to (circulation) baseline.
What's your experience with food-based vitamin C?

I don't consciously take the enzymes away from vitamin C. But since I already have normal serum iron, I don't see why iron would be leached out with the lysing of plaque. Plus, wouldn't the bacteria and iron in plaque already have begun to do damage already?

I haven't been a fan on food-based vitamin C, although I imagine I would be having some as I would eat plenty of fruits for the potassium.

 

[yerrag]

..too high total bodywater?
whats your weight,height approx bodyfatmass,etc

It isnt about Fluid dynamics in hypertension in my opinion,although in general Blood-Pressure Point measure it is.But Hypertension is not higher Bloodpressure moving along a line until it is too high,it is symptomatology of whole body inflammation,with hypertension as a biological sign on top,signifying.
it is a inflammtory condition.
It decreases eNOS and Arginase,something like Viagra is doing it more locally diametrically.


Either you have too much fluid in the active circulation,or weigh down and compression of your venous system through physical weight and concomitant tissue compression,Or vascular reduction in circumference by the Anti-Viagra-Effect
of NaCl,by virtue of induction of Th17-Inflammation,which reduces needed(no one says CO2 please!)eNOS-
availability,thus lowering needed local NO,delivered to us by eNOS.


Also,you have accrued an large amount of sodium already,so it takes a couple of months to come off of excess.
Humans are highly,highly competent to retain Sodium,Peat didnt read or understood the World-Literature in that
regard.
Maybe he is inferring from his own experience,but the literature is ruled by different thought.Maybe they are right,?

I read a lot of Observations and Experiences of actual Hands-On clinicians and active researchers.
We are taking Supraphysiologic amount of NaCl in,and all we have to show for it is stale Angiotensin and Aldosterone-
hydraulics.Salt Loading is over.

Thanks, but it's hard for me to see the relationship of salt to high blood pressure in my case. I've not been particularly high on salt, and neither do I consciously seek to have low-salt in what I eat. It has been this way ever since I can remember. I can't see any reason for my body to react differently to salt at any given point in my life, such that it would be accounting for my high blood pressure condition. If your hunch is correct, then I would be seeing the same symptoms with my siblings, who share a similar taste and food preference. I am alone among eight to have high blood pressure.

I have tried increasing salt intake, taking 2 tablespoons in one sitting, with water, and this had no noticeable effect on me, even on blood pressure. I did it for a day only though, but I stopped only because it did not lower my blood pressure, not one iota. I'm slowly increasing my salt intake, currently by taking 3 grams each day to slowly increase my blood volume. It isn't increasing my blood pressure and neither is it decreasing it.

In my situation where my RBC, hemoglobin, and hematocrit are high enough to lead me to conclude that I have low blood volume (aka dehydration), reducing salt intake is no way to increase my blood volume, and runs counter to the direction I'm in.

 

[yerrag]

My RBC jumped from 5.28 to 5.71, Hemoglobin from 154 to 168, and Hematocrit from 0.45 to 0.48, compared to 2 months ago; my low blood volume grew even worse. This is indicative of low serum albumin that got worse. While my serum albumin would appear to be unchanged, compared to 5 months ago, from 4.19 to 4.27 g/L, I have to take into account that in terms of total albumin, my serum albumin has gone down because the blood volume has gone down. Since total serum albumin plays a huge role in determining the blood volume, low total serum albumin would cause blood pressure to go up, as lower blood volume (from lower serum albumin) causes higher blood pressure to compensate for it.

The optimal range for RBC is 4.2 to 4.9, and my RBC is 5.71. This means my RBC is .81 above range. At the very least, my blood volume is 4.9/5.71 or just 85 percent of normal.

Adjusting for this, my effective serum albumin would be 4.27 (.85) =3.62 g/L, which is below optimal range of 4.0-5.0. The implication is that, given the low serum albumin, my blood cannot hold on to salt well, and this makes it difficult to increase blood volume. The first order of business is to increase serum albumin. I have to eat more protein, so that the liver can produce more albumin. But this isn't enough. Assuming I'm right in my suspicion that albumin is being used up to bind endotoxins, I will have to find a way for endotoxins to be bound and excreted without using up albumin. Or if endotoxin is not being bound and excreted, it would have to be deactivated somehow. While this forum makes mention of many substances (pregnenolone, DHEA, progesterone, methylene blue, vitamin C, vitamin A, glycine, riboflavin), a lot of it (except progesterone, which deactivates it) is mostly about TLR4 antagonism. Chylomicrons and HDL transports endotoxin to the liver, where it is detoxified and included in bile for fecal excretion (unless the bile is used to emulsify fats, whereupon it gets into chylomicrons. Ray Peat says that insoluble fibers in the gut absorbs endotoxins, and this keeps it from being recycled back). While I haven't read about endotoxins being excreted through urine, I suspect it does as I experienced extreme urination frequency after taking proteolytic enzymes, and I believe it was the endotoxins being released by the lysis of plaque. The albumin binding endotoxins into a lipid binding protein (LBP), or a version of it, was being urinated, and this has led to my serum albumin and blood volume being lowered significantly, to such extent that it resulted in a further increase in my already high blood pressure.

I am of the opinion that the above-mentioned substances (pregnenolone etc.) aren't going to help me effectively deal with endotoxins in the way that it won't keep robbing me of the vital albumin needed to build up my blood volume and in doing so, would bring a significant lowering of my blood pressure. Getting the right dosage is problematic, much less getting the right combination of substances at the right dosage for each substance. This is also compounded by the fact that endotoxins come in many flavors, and getting a combo that works would be very context-specific for each individual. I am hoping though that a solution for me will come in the form of a blend of Chinese herbs, and I'm waiting for my order of Chinese herbs to arrive.

On my high serum creatinine value of 1.47, I can take solace in the fact that this appears that high because the low blood volume makes it go higher. If I were to use the range of 4.2 - 4.9 as my optimal range for RBC, and given my current RBC is 5.71, and adjusting for normal blood volume, I would still be getting an effective serum creatinine value ranging from 1.08 to 1.26. This is much lower, and at the lower range puts me just below chronic kidney disease territory. Clearly, more needs to be done. And I'm hoping that once my blood volume is restored back to normal, I can continue to lyse my plaque to such extent that I can recover the lost filtering ability of my kidneys.

 

[Amazoniac]

I wasn't going regularly to the dentist for oral prophylaxis. I was just brushing my teeth and flossing regularly. It wasn't enough as plaque forms easily on my teeth. My teeth probably leeches also, due to poor calcium intake. So my dental enamel wasn't a particularly strong barrier to endotoxins penetrating into teeth around the gumline, and endotoxins could easily be followed by infection.


I don't consciously take the enzymes away from vitamin C. But since I already have normal serum iron, I don't see why iron would be leached out with the lysing of plaque. Plus, wouldn't the bacteria and iron in plaque already have begun to do damage already?

I haven't been a fan on food-based vitamin C, although I imagine I would be having some as I would eat plenty of fruits for the potassium.

I was curious if it had an effect, didn't mean sequestered metals by bacteria, I meant their release in general. It can help dissolve fibrin where it's not desired, but it may also be counterproductive where it's needed. The higher the circulating dose of both, the more likely it is for adverse reactions to occur. And I'm not yet confident that synthetic ascorbic acid is as stable as that from food, ascorbate circulates freely.

What's your experience with other forms of vitamin K? You use mk-4 and venom D on a daily basis? How? This is more out of curiosity.
Also, how living in a cold climate and not supplementing vitamin C would affect you?


This might interest you (not calling you a chicken, you're a fish with feelings):

- Impact of Serratiopeptidase Treatment on Performance and Health Parameters in Broiler Chickens

"The experimental design appears as if it was lacking a 5th group that should have been treated with the enzyme serrapeptase, but the reason that we did not include this group that the product manufacturer stated that this enzyme is not used alone but it should be always used in combination with antibiotics in case of treatment of bacterial infection as it is does not have an antibacterial properties."


Unfortunately such group would make a difference in interpretation, they should've included one with just the antibiotic. But at least its concentration in water was fixed while the serrating toxin varied.

Assuming that water intake was similar, it was the infection the responsible for elevating liver enzymes and the toxin didn't appear to elevate it. The living conditions appeared to be atrocious, kind people. It can confound because the antibiotic could lower the enzymes below control values at the same time that the toxin increases, making it look like it didn't impact.

Perhaps it's worth blood-testing yourself with and without the doxycycline use.​

Spoiler

- water input output body | Google
- Water Consumption Behavior in Broilers

Regarding the amines mentioned:

- Production, purification, characterization, immobilization, and application of Serrapeptase: a review (posted on the other thread)

"Serrapeptase reduces pain by restricting the inflamed tissues from releasing pain-inducing amines such as bradykinin (Mazzone et al., 1990). It can also hydrolyze bradykinin, histamine and serotonin, which are responsible for oedemic responses (Malshe, 2000)."​

 

[yerrag]

I was curious if it had an effect, didn't mean sequestered metals by bacteria, I meant their release in general. It can help dissolve fibrin where it's not desired, but it may also be counterproductive where it's needed. The higher the circulating dose of both, the more likely it is for adverse reactions to occur. And I'm not yet confident that synthetic ascorbic acid is as stable as that from food, ascorbate circulates freely.

My last test on ferritin showed it had come down, compared to last year when I had not have my periodontal-infected teeth (two of them) extracted. My last test, early February this year, was before I started using enzymes. I attribute the lower ferritin from lower bacteria levels, as the source of bacteria had been taken care of. But I haven't tested my ferritin, TIBC, and serum iron lately. If bacteria is being released from lysing plaque, my ferritin level would increase. If it's both bacteria and iron being released, ferritin would increase further. Either way, I wouldn't release know if iron were being released.

What exactly does vitamin C do to iron? Does it cause increased uptake of iron from the gut? Or does it caused increased uptake of iron into the cell? If it's the former, then it doesn't matter. If it's the latter, then it matters, and since I don't take vitamin C after meals, my vitamin C intake won't really increase iron absorption from the gut into the bloodstream.

I'm not following you on the distinction between natural and synthetic vitamin C in terms of stability. Can you elaborate?

This might interest you (not calling you a chicken, you're a fish with feelings):

- Impact of Serratiopeptidase Treatment on Performance and Health Parameters in Broiler Chickens

"The experimental design appears as if it was lacking a 5th group that should have been treated with the enzyme serrapeptase, but the reason that we did not include this group that the product manufacturer stated that this enzyme is not used alone but it should be always used in combination with antibiotics in case of treatment of bacterial infection as it is does not have an antibacterial properties."


Unfortunately such group would make a difference in interpretation, they should've included one with just the antibiotic. But at least its concentration in water was fixed while the serrating toxin varied.

Assuming that water intake was similar, it was the infection the responsible for elevating liver enzymes and the toxin didn't appear to elevate it. The living conditions appeared to be atrocious, kind people. It can confound because the antibiotic could lower the enzymes below control values at the same time that the toxin increases, making it look like it didn't impact.

Perhaps it's worth blood-testing yourself with and without the doxycycline use.

The only thing I see noteworthy is that the use of serrapeptidase on these chickens caused the chickens to gain weight. It's funny as this is a positive thing for the chicken raisers, but if I gained weight it's not a positive thing. But the reality is that the serrapeptidase is causing weight gain. Study does not dwelve into why.

But you made me look into my doxycycline usage.

At a low dose of 40 mg/day for a month, my seborrheic dermatitis was gone.

This was followed by a month where I just used the proteolytic enzyme ZymEssence for a month, and I seemed to do well. There was an increase in bacteria, as seen in higher wbc (7.38) and neutrophil (71.30), but there was a reduction in endotoxins, as seen in lower serum monocyte readings (5.80).

This was followed by a week where I continued to take ZymEssence but added 2x100mg of doxycycline daily. I began to urinate a lot. My bacteria went down, as seen in lower wbc (6.98) and neutrophils (65.0), but my endotoxins went up, as seen in higher monocytes (8.20).

The following week, I lowered doxy to 100mg/day, while continuing to take ZymEssence. My heavy urination still continued. My bacteria went further down (wbc- 6.67, neutrophil-67.1), and my endotoxins went down, with monocytes at 6.0. I developed a hip pain at this point, which I believe to be endotoxin-related. The pain persists till now, 4 months and counting.

I then stopped all enzymes and antibiotics the following week. I took Serrapeptidase 120,000 SPU for 3x for only one day. Then, five days later, I had my blood tested. My bacteria skyrocketed. My wbc was 11.34, and my neutrophils was 81. Yet my endotoxins went down, as monocyte went down to 5.60.

Now, everything seems to be falling into place. It's good you made me look again, as this time I can see what I missed earlier- 4 months ago!

- I do well with doxycyline at 40mg/day. It was able to lower bacteria such that my seborrheic dermatitis cleared. It wasn't creating an endotoxin load that my body can't handle. Doxycyline at 100mg/day or more is too much for my body to handle, as far as endotoxin is concerned.

- Whether I was using ZymEssence or serrapeptidase, the lysing of plaque was only releasing bacteria, and not endotoxins.

-Taking ZymEssence at 3x/day was releasing bacteria at a manageable rate, but taking the 120,000 SPU serrapeptidase 3x/day just for a day, was enough to release a load of bacteria. Just a day of serrapeptidase 120k spu taken 3x results in wbc and neutrophils of 11.34 and 81, whereas a week of ZymEssence taken 3x/day results only in wbc and neutrophils of 6.67 and 67.1.

-It was the use of doxycycline at 200mg/day (and maybe also 100mg/day) that would result in very heavy urination, as the die-off or endotoxins was causing the high urination rate.

As I consider the ramifications of what I just concluded, I realize that I have to go back to my notes from early July to now, to see what led to my increase in blood pressure and its persistent stay in that high range. I think I know the answer. There was a lot of endotoxin that needed to be expelled, and it took away a lot of my serum albumin along with its excretion in urine. This resulted in lower blood volume, and this is seen in much higher serum RBC, hemoglobin, and hematocrit readings. Since blood volume does not change so much rapidly, it explains why my blood pressure has consistently remained high.

In my case, where I have lots of embedded and dormant bacteria in my vascular plaque, too high a dose of doxycycline should be avoided. I can continue using ZymEssence at 3x/day, but serrapeptase 12ok spu should be used sparingly or avoided if ZymEssence can already do the job adequately.

 

[Amazoniac]

My last test on ferritin showed it had come down, compared to last year when I had not have my periodontal-infected teeth (two of them) extracted. My last test, early February this year, was before I started using enzymes. I attribute the lower ferritin from lower bacteria levels, as the source of bacteria had been taken care of. But I haven't tested my ferritin, TIBC, and serum iron lately. If bacteria is being released from lysing plaque, my ferritin level would increase. If it's both bacteria and iron being released, ferritin would increase further. Either way, I wouldn't release know if iron were being released.

What exactly does vitamin C do to iron? Does it cause increased uptake of iron from the gut? Or does it caused increased uptake of iron into the cell? If it's the former, then it doesn't matter. If it's the latter, then it matters, and since I don't take vitamin C after meals, my vitamin C intake won't really increase iron absorption from the gut into the bloodstream.

I'm not following you on the distinction between natural and synthetic vitamin C in terms of stability. Can you elaborate?

It's not that. The little iron that's free or perhaps loosely-bound from the activity of the enzyme might interact with extra vitamin C in the circulation, triggering then a phantom reaction. Which is why I wondered if there could be differences if they're taken apart.

What makes iron protected in the food might help when it's metabolized in the body, flavonoids are examples that have chelating properties.

Since the saw is used in degenerative brain issues, it's unlikely for it to make it worse, but given that there's no risk involved and that you use a synthetic product, I would be curious to compare if it was me.

The only thing I see noteworthy is that the use of serrapeptidase on these chickens caused the chickens to gain weight. It's funny as this is a positive thing for the chicken raisers, but if I gained weight it's not a positive thing. But the reality is that the serrapeptidase is causing weight gain. Study does not dwelve into why.

The difference wasn't significant.

Spoiler

The following is remarkable:

Spoiler

I haven't stop to consider dose equivalences, but 1-2 g/L doesn't seem low.

But you made me look into my doxycycline usage.

At a low dose of 40 mg/day for a month, my seborrheic dermatitis was gone.

This was followed by a month where I just used the proteolytic enzyme ZymEssence for a month, and I seemed to do well. There was an increase in bacteria, as seen in higher wbc (7.38) and neutrophil (71.30), but there was a reduction in endotoxins, as seen in lower serum monocyte readings (5.80).

This was followed by a week where I continued to take ZymEssence but added 2x100mg of doxycycline daily. I began to urinate a lot. My bacteria went down, as seen in lower wbc (6.98) and neutrophils (65.0), but my endotoxins went up, as seen in higher monocytes (8.20).

The following week, I lowered doxy to 100mg/day, while continuing to take ZymEssence. My heavy urination still continued. My bacteria went further down (wbc- 6.67, neutrophil-67.1), and my endotoxins went down, with monocytes at 6.0. I developed a hip pain at this point, which I believe to be endotoxin-related. The pain persists till now, 4 months and counting.

I then stopped all enzymes and antibiotics the following week. I took Serrapeptidase 120,000 SPU for 3x for only one day. Then, five days later, I had my blood tested. My bacteria skyrocketed. My wbc was 11.34, and my neutrophils was 81. Yet my endotoxins went down, as monocyte went down to 5.60.

Now, everything seems to be falling into place. It's good you made me look again, as this time I can see what I missed earlier- 4 months ago!

- I do well with doxycyline at 40mg/day. It was able to lower bacteria such that my seborrheic dermatitis cleared. It wasn't creating an endotoxin load that my body can't handle. Doxycyline at 100mg/day or more is too much for my body to handle, as far as endotoxin is concerned.

- Whether I was using ZymEssence or serrapeptidase, the lysing of plaque was only releasing bacteria, and not endotoxins.

-Taking ZymEssence at 3x/day was releasing bacteria at a manageable rate, but taking the 120,000 SPU serrapeptidase 3x/day just for a day, was enough to release a load of bacteria. Just a day of serrapeptidase 120k spu taken 3x results in wbc and neutrophils of 11.34 and 81, whereas a week of ZymEssence taken 3x/day results only in wbc and neutrophils of 6.67 and 67.1.

-It was the use of doxycycline at 200mg/day (and maybe also 100mg/day) that would result in very heavy urination, as the die-off or endotoxins was causing the high urination rate.

As I consider the ramifications of what I just concluded, I realize that I have to go back to my notes from early July to now, to see what led to my increase in blood pressure and its persistent stay in that high range. I think I know the answer. There was a lot of endotoxin that needed to be expelled, and it took away a lot of my serum albumin along with its excretion in urine. This resulted in lower blood volume, and this is seen in much higher serum RBC, hemoglobin, and hematocrit readings. Since blood volume does not change so much rapidly, it explains why my blood pressure has consistently remained high.

In my case, where I have lots of embedded and dormant bacteria in my vascular plaque, too high a dose of doxycycline should be avoided. I can continue using ZymEssence at 3x/day, but serrapeptase 12ok spu should be used sparingly or avoided if ZymEssence can already do the job adequately.

Fish, I think it would be helpful for you to start graphing these, it's going to make it easier for you and others to grasp what's happening. It was fast to do it, and with the detailed information that you have, it's possible to make it more accurate and it can be elucidating.

Spoiler

- Herb, Nutrient, and Drug Interactions: Clinical Implications and Therapeutic Strategies (978-0323029643)

"The several mechanisms of interaction between the tetracycline class of antibiotics and folic acid are complex and conflicting, depending on dose, duration, timing, and patient characteristics. Folic acid may interfere with the absorption and effectiveness of tetracycline antibiotics if ingested simultaneously, and vice versa.[360] Tetracyclines inhibit bacterial protein synthesis by binding to the 30S ribosome, blocking access of the aminoacyl tRNAs at the ‘‘A’’ acceptor site on the mRNA-ribosome complex. These drugs may interfere with the activity and induce the depletion of folic acid and other nutrients, particularly other B vitamins.[361] Additionally, extended or recurrent use of antibiotics can cause folate depletion by eliminating the healthy intestinal flora, a major source of endogenous biosynthesis of folate (and B12).[362,363] Many patients with conditions for which tetracyclines are prescribed have depleted folate nutriture."

"Omray and Varma[360] demonstrated that oral administration of a vitamin C- and vitamin B-complex formulation could impair absorption and reduce bioavailability of tetracycline hydrochloride through pharmacokinetic interference. However, numerous clinicians and authors fail to mention such risks or advise appropriate corrective measures in discussions of coadministration of these agents. Some patient populations receiving antibiotic therapy have
pathophysiological conditions, medical history, and lifestyle/dietary factors characterized by malnutrition, malabsorption, or nutrient depletion."

"Similarly, in a discussion of several cases of tropical sprue among indigenous patients in Australia, with a history of excessive alcohol intake and characterized by alteration in the intestinal microflora, overgrowth of coliform bacteria, mucosal damage and malabsorption, and protein loss, Hanson[366] recommended that concomitant tetracycline use, specifically doxycycline, and folic acid therapy ‘‘can be rapidly and dramatically effective, although the tetracycline course should continue for 3-6 months.’’

Note: Falsely low serum folate concentrations may occur with the Lactobacillus casei assay method in patients receiving tetracycline therapy."

"Physicians prescribing tetracycline antimicrobials, repeatedly or for more than 2 weeks, are advised to coadminister folic acid; a moderate supplemental dose of 400 to 800 mg/day typically is adequate. These levels may also be obtained through a diet rich in leafy green vegetables, beans, beets, citrus, meat, and wheat germ. The importance of such nutrient support is amplified in pregnant women and individuals with compromised nutritional status or a history of high alcohol intake."

"Coadministration of probiotic flora along with vitamins B12 and K is usually appropriate. The aim of an integrative approach combining tetracycline, folate, and vitamin B12 is to restore intestinal mucosal structure, normalize absorptive function, correct folate and B12 deficiencies, and correct any macrocytic anemia.

In most patients, only the probiotic flora are appropriate when a shorter course of a tetracycline (7-10 days) is administered as a countermeasure to the antibiotic-induced disruption of healthy intestinal ecology. Regular supplementation with vigorous cultures of Lactobacillus acidophilus, Bifidobacterium bifidus, and other probiotic bacteria for 2 to 4 weeks can safely and effectively preclude or reverse subsequent antibiotic-induced folate depletion; up to 6 months of probiotic intake may be necessary to fully reestablish the symbiotic intestinal flora in patients receiving more than one course of antibiotics.

"Tetracycline should be administered at least 2 hours before or 4 hours after oral intake of folic acid, alone or as part of a B-complex or multivitamin formulation, to avoid interference with gastric absorption. Evidence for such an adverse interaction is minimal, but prudence suggests that such simple precautions may be beneficial."​

- Drug-induced Nutrient Depletion - Life Extension
- Handbook of Drug-Nutrient Interactions (978-1-60327-362-6)

 

[yerrag]

It's not that. The little iron that's free or perhaps loosely-bound from the activity of the enzyme might interact with extra vitamin C in the circulation, triggering then a phantom reaction.

What is this phantom reaction you speak of?

Since the saw is used in degenerative brain issues, it's unlikely for it to make it worse, but given that there's no risk involved and that you use a synthetic product, I would be curious to compare if it was me.

I'm not following. Do you literally mean a saw?

The difference wasn't significant.

Spoiler

The following is remarkable:

Spoiler

I haven't stop to consider dose equivalences, but 1-2 g/L doesn't seem low.

I only read the abstract, and it didn't talk about the anti-inflammatory effect of serrapeptidase. That changes the picture, as now I see the weight gain, and improved FCR as a positive now. Thanks, as I had forgotten totally about the anti-inflammatory effect of proteolytic enzymes, being that I got so focused on its plaque-lysing abilities as well as the attendant release of bacteria from distintegrating plaque.

Fish, I think it would be helpful for you to start graphing these, it's going to make it easier for you and others to grasp what's happening. It was fast to do it, and with the detailed information that you have, it's possible to make it more accurate and it can be elucidating.

Spoiler

Nice graph. I can see how helpful the graphs can be. I'm tempted to do them, but on the other hand, I've become a "conclusion reader" of studies and think I might as well be a "conclusion writer." And a person who skips graphs like me could still get away with reading the conclusions, and I laid my conclusions as clear as i can.