If urine is too acidic in the evening (lower than 5.5 IME) it is a bad sign. But the bicarb mouth swish is a good test as well.
There are two parts to the swab. One part matched up to where it said 6.5 the other matched the 5.0-5.5.
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If urine is too acidic in the evening (lower than 5.5 IME) it is a bad sign. But the bicarb mouth swish is a good test as well.
Sorry, I don't get it how it can give two different results at the same time.There are two parts to the swab. One part matched up to where it said 6.5 the other matched the 5.0-5.5.
Sorry, I don't get it how it can give two different results at the same time.
If you have bicarb at home do the mouth swish and spit it out. It is harmless and will help you gauge the need for an alkalizing protocol. Be warned that it can cause a candida flare in those who have candida overgrowth. But it does relieve ammonia.
You can do a 15 minute foot soak or use bicarb as a shower scrub. It is very relaxing. When my urine pH tested 4.5 I took a bicarb bath with 1/2 cup of bicarb in water and slept wonderfully.
A couple of weeks ago when my ammonia was high again from upping my T3 I took a bicarb bath and felt wonderful the following day after a perfect night of sleep.
Definetely confusing. Trust your mouth swish. Alternatively or additionally, S. boulardii also help.The Strips are like these . There are 2 color pads on each stick.
Have you tested with strips before and after the foot soak to see how much your pH rises?You can do a 15 minute foot soak
When I first took a bicarb bath it was 4.5 in the evening before the bath. In the following evening it was 6 (at the same time of the day).Have you tested with strips before and after the foot soak to see how much your pH rises?
When the basic purine structure is oxidized, it becomes in turn hypoxanthine, xanthine, and uric acid, by the addition of oxygen atoms. When methyl groups (CH3) are added to nitrogens in the purine ring, the molecule becomes less water soluble.
Nucleosides Nucleotides Nucleic Acids. 2008 Aug; 27(8): 967–978.
Inactivation of Nitric Oxide by Uric Acid
Christine Gersch,1 Sergiu P. Palii,1 Kyung Mee Kim,1 Alexander Angerhofer,2 Richard J. Johnson,1 and George N. Henderson1,3,4
1Division of Nephrology and Hypertension, Department of Medicine, University of Florida, Gainesville, Florida, USA
2Department of Chemistry, College of Liberal Arts and Sciences, University of Florida, Gainesville, Florida, USA
3Division of Endocrinology and Metabolism, Department of Medicine, College of Medicine, University of Florida, Gainesville, Florida, USA
4General Clinical Research Center, University of Florida, Gainesville, Florida, USA
Abstract
The 1980 identification of nitric oxide (NO) as an endothelial cell-derived relaxing factor resulted in an unprecedented biomedical research of NO and established NO as one of the most important cardiovascular, nervous and immune system regulatory molecule. A reduction in endothelial cell NO levels leading to “endothelial dysfunction” has been identified as a key pathogenic event preceding the development of hypertension, metabolic syndrome, and cardiovascular disease. The reduction in endothelial NO in cardiovascular disease has been attributed to the action of oxidants that either directly react with NO or uncouple its substrate enzyme.
In this report, we demonstrate that uric acid (UA), the most abundant antioxidant in plasma, reacts directly with NO in a rapid irreversible reaction resulting in the formation of 6-aminouracil and depletion of NO.
We further show that this reaction occurs preferentially with NO even in the presence of oxidants peroxynitrite and hydrogen peroxide and that the reaction is at least partially blocked by glutathione.
This study shows a potential mechanism by which UA may deplete NO and cause endothelial dysfunction, particularly under conditions of oxidative stress in which UA is elevated and intracellular glutathione is depleted.
Clin Exp Rheumatol. 2001 Nov-Dec;19(6):661-5.
Hyperuricemia and gout in thyroid endocrine disorders.
Giordano N1, Santacroce C, Mattii G, Geraci S, Amendola A, Gennari C.
Author information
Abstract
OBJECTIVE:
A significant correlation between thyroid function and purine nucleotide metabolism has been established in hypothyroidism. On the contrary, the relationship between hyperthyroidism and purine metabolism is more controversial. The present study evaluates the prevalence of hyperuricemia and gout in patients affected by primary hypothyroidism and hyperthyroidism.
METHODS:
We studied 28 patients with primary hypothyroidism and 18 patients with primary hyperthyroidism, all hospitalized because of endocrine dysfunction. All underwent a series of clinical, biochemical and instrumental evaluations; in particular, thyroid-stimulatin hormone (TSH), free thyroxine (fT4), blood urea, serum creatinine, creatinine clearance, serum and urinary uric acid levels were measured.
RESULTS:
In comparison to the prevalence reported in the general population, a significant increase of both hyperuricemia and gout was found in the hypothyroid patients, and of hyperuricemia in the hyperthyroid patients. In hyperthyroidism the hyperuricemia is due to the increased urate production, while in hypothyroidism the hyperuricemia is secondary to a decreased renal plasma flow and impaired glomerular filtration.
CONCLUSIONS:
Our findings confirm the data in the literature concerning the high prevalence of hyperuricemia and gout in hypothyroidism. It shows that hyperthyroidism can cause a significant increase in serum uric acid, as well, although lower than the hyperuricemia due to thyroid hormone deficiency.
Sometime ago I read a really interesting info about it here but now it is asking for a sign up...
Curbing Fructose Intake May Decrease Elevated Uric Acid
Elevated uric acid levels are associated with increased risks for hypertension, gout, and renal impairment.
http://www.renalandurologynews.com/...y-decrease-elevated-uric-acid/article/309628/
Glycinate, aspartate, citrate and sulfate made me feel worse.Gondwanaland, have you tried other forms of magnesium besides the oxide form? Or is there a reason that magnesium oxide would be more helpful?
I think the basic chemistry is that oxide turns into OH and neutralizes the potential acidic urate salts.Or is there a reason that magnesium oxide would be more helpful?
I think the basic chemistry is that oxide turns into OH and neutralizes the potential acidic urate salts.
No, thanks for the recommendation.Have you read Alexander Haig's online books on uric acid? "Uric Acid as a factor in the causation of disease" is my favorite.
No ideaAnd have you ever wondered what's in that one joint where the uric acid settles and causes pain?
No, thanks for the recommendation.
No idea
What I have seen when I look around is an immense effort to RAISE uric acid... Ray Peat and his followers, and Kimsie protocols here at PR.
Exactly, to benefit from what you just said...The inability to get rid of uric acid is a disorder in the UA metabolism...Yikes, raise uric acid levels?
In the 1st page of this thread I linked a study recommending potassium citrate for this since sodium urate might be counter-productive.You are on to something with the sodium bicarb because it keeps the urine alkaline enough to remove excess uric acid from the body.