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I'm feeling very stupid (please stop the cries of “Figures!”)
I must have had pH on my mind when I woke this morning. A not-so-common complaint, probably caused by seemingly endless discussions about the effects of food on pH.
My stance is that an alkalizing diet can benefit gouties by reducing the risk of uric acid stones in the kidneys. I could see little other potential benefit, because our bodies maintain fairly constant blood pH, so it is not possible to raise blood alkalinity in the hope of making uric acid more soluble.
Somehow, the thought popped into my mind: “Yes, we test uric acid in the blood as a measure of how much at risk we are of a gout attack, but gout crystals do not form in the blood, they form [mainly] in the joints”
A quick look at one report (On the viscosity and pH of synovial fluid and the pH of blood. Jebens & Monk-Jones) reveals to me that synovial fluid pH can range from 6.5 to 8.9!
So now, I have more questions than answers:
- Can the range be even wider?
- What influences the pH of synovial fluid?
- Do rheumatologists routinely measure pH of synovial fluid?
- How much does uric acid solubility change with pH?
- Have I been asleep when this has been discussed before, or is it new ground?
Any and all contributions very gratefully received.
Yep,
that's very interesting.
With that pH swing of 6.5 to 8.9 I doubt that it has to be any larger…that range is a hydrogen ion content of several hundredfold.
I've mentioned it occasionally but with little emphasis as in “who knows what the temperature and pH of the affected joints are.”
Hmm,
Uric acid solubility with pH? Let's see what I can dig up without running into $$$$$Springer links$$$.
One of the problems seems to be the relationship between uric acid and monosodium urate…both of which present gout problems and each has it's own relationship to pH.
Then there is the other quirk of uric acid solutions:
As much as 220 mg./dl. of uric acid could be dissolved for 24 hours at pH 7.0. But following seven-day incubation the total dissolved urate concentration decreased to 16 mg./dl. due to NaU crystallization. The stability of NaU supersaturation depended not only on the concentration of sodium and urate anion but also on time and pH.
There is this strange TIME relationship. Might explain a bit why a high concentration or urate after exercise doesn't cause pain til the next morning.
Let me add another bugaboo to your good questions:
Is there anything we can do with diet to change the pH of our synovial fluid?
As an overview to this question, perhaps gout is a disease ultimately caused by too acidic a synovial fluid. As as adjunct, long ago I read a good long article (on paper actually) about how colchicine worked and why it was so specific to gout. THe writer said with some certainty that colchicine alkalyzed the synovial fluid. Sounds logical to me.
And appropos of nothing: I found that the SKIN is a rather acidic 5.5.
I suspect that diet affects the Ph level in joint fluid, from my recent experiences where my SUA went up to 7.5 after being much lower in a stricter diet phase , with no hint of a gout flare/attack.
Blood and saliva Ph may well stay pretty constant, but urine values go all over the place during the day, for sure.
Interesting to see actual values in joints here [& surprisingly alkaline!] – I suppose the reason why it changes is sinovial fluid doesn't get directly regulated by blood flow through the liver.
White blood cells have a certain delay in action as noticed on a first infection- and the need for antibiotics as a standby cure. [This would explain time delay in gout kicking in]
Many times, it's the body doing the work – but who can tell once the drug has been started?
This is one reason why staying off meds helps find out what's really going on inside- but hard to do without a lab on standby and medics gagging for the results! Some chance.
trev said:
Post edited 2:16 pm – March 22, 2010 by trev
I suspect that diet affects the Ph level in joint fluid, from my recent experiences where my SUA went up to 7.5 after being much lower in a stricter diet phase , with no hint of a gout flare/attack.
I'm experiencing much same thing at the moment: yesterday & today's readings 8.9 & 8.5
with absolutely no sign of a flare, twinges.. nada. Can't work out what's going on, except I had a very physical day on Sat & got pretty dehydrated. I've been drinking more, obviously, but I guess UA levels fall a lot slower than they rise. I'm going to monitor daily this week to see how that theory pans out.But anyway, go herbs!
There's another factor which may be significant: I'm experiencing a minor flare up of colitis at the moment, no doubt due to high stress levels over the past couple of months with no let up in pressure due till Aug. It's been in remission for about 5 yrs, so I was not pleased to see another 'old friend' making a reappearance. I'm pretty sure that 10 yrs of meds (mesalazine) for that was a factor in knackering my kidneys. But I haven't worked out a connection between colitis & gout yet. If anything, I would have thought it would help: poor fat absorption, increased urination/defecation. Will probably go and get my herb prescription adjusted on Fri.
I meant to add for Zip, that the skin is acidic to fight off infections. There's apparantly a surprising amount of bacteria floating about, that we resist daily.
This may be a reason why the body doesn't 'normally' mind high acidic levels in the blood as well, but in Gouts case this is a 'blessing too far' !
zip2play said:
Post edited 12:58 pm – March 22, 2010 by zip2play
Yep,
that's very interesting.
With that pH swing of 6.5 to 8.9 I doubt that it has to be any larger…that range is a hydrogen ion content of several hundredfold.
I've mentioned it occasionally but with little emphasis as in “who knows what the temperature and pH of the affected joints are.”
Hmm,
Uric acid solubility with pH? Let's see what I can dig up without running into $$$$$Springer links$$$.
One of the problems seems to be the relationship between uric acid and monosodium urate…both of which present gout problems and each has it's own relationship to pH.
Then there is the other quirk of uric acid solutions:
As much as 220 mg./dl. of uric acid could be dissolved for 24 hours at pH 7.0. But following seven-day incubation the total dissolved urate concentration decreased to 16 mg./dl. due to NaU crystallization. The stability of NaU supersaturation depended not only on the concentration of sodium and urate anion but also on time and pH.
There is this strange TIME relationship. Might explain a bit why a high concentration or urate after exercise doesn't cause pain til the next morning.
Let me add another bugaboo to your good questions:
Is there anything we can do with diet to change the pH of our synovial fluid?
As an overview to this question, perhaps gout is a disease ultimately caused by too acidic a synovial fluid. As as adjunct, long ago I read a good long article (on paper actually) about how colchicine worked and why it was so specific to gout. THe writer said with some certainty that colchicine alkalyzed the synovial fluid. Sounds logical to me.
And appropos of nothing: I found that the SKIN is a rather acidic 5.5.
Zip, you opened up another BIG can of worms, so I'll start a new link under: Uric Acid and Mono Sodium Urate.
zip2play said:
As an overview to this question, perhaps gout is a disease ultimately caused by too acidic a synovial fluid. As as adjunct, long ago I read a good long article (on paper actually) about how colchicine worked and why it was so specific to gout. THe writer said with some certainty that colchicine alkalyzed the synovial fluid. Sounds logical to me.
And another “side” to this: inflammation tends to lower pH in the affected area as acids are released by White Blood Cells during their attack on urate crystals. I imagine this must increase the risk of additional urate crystals forming.
Similar to colchicine, I've seen a study that shows how steroid injections lower acidity of synovial fluid, despite the injection being an acid. Tests showed immediate lowering of pH as the acidic steroid hits, then gradual increase over (from memory) 72 hours as the medication reduces inflammation.
Interesting stuff, this organic chemistry / microbiology.
Hard to search for though, in this instance. It seems many researchers have the initials PH, and many more have PH.Ds
The whole problem of gout study is that researchers watch medium to long term 'cause and effect ' and Gouties deal ing with the day to day reactions of their bodies to SUA levels and their response to this, with many complex personal variables.
Three groups referenced on here – New age nutters (seemingly?) , puzzled 'middle men' crunching meds and aloof researchers trying to make a name/living out of universal pain.
Is there a common language?
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