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Gout
- Thread starter Bruv
- Start date
Update. I have been having about half a teaspoon of bicarbonate of soda in my orange juice every morning since just after the making the post above. I have also started having nearly half a teaspoon of tart cherry powder most evenings. The gout seems to be easing up.
@Bruv, more than two years later ... has your gout completely subsided after further continuing the baking soda (and possibly tart cherry powder)? ... Did you develop gout again, maybe at other places (e.g., fingers), after discontinuation?
Interesting to read about the baking soda connection. In a newer post, @judge also reported it to be very effective in relieving gout-related inflammation.
Interesting to read about the baking soda connection. In a newer post, @judge also reported it to be very effective in relieving gout-related inflammation.
@marteagal The gout has come back at times but only when I have either got lazy about the bicarbonate of soda or run out of it and forgotten to replace it. It started flaring up again the other week. We had no bicarbonate of soda in the house so I was adding a little soda water to my OJ and this seemed to help. I'm back on the bicarbonate of soda and I think this is starting to work again.
I have found cherries very helpful for this too (I must remember to buy some!). Even cherries from a jar have been good in the past (About a dozen cherries per day). I was looking at cherry powders on ebay etc the other day but I will probably go with fresh cherries if I find some nice ones.
I have found cherries very helpful for this too (I must remember to buy some!). Even cherries from a jar have been good in the past (About a dozen cherries per day). I was looking at cherry powders on ebay etc the other day but I will probably go with fresh cherries if I find some nice ones.
I'll sometimes have less with with my orange juice but just have more servings over the course of the day. Half a teaspoon makes the orange juice fizz up a lot so if you don't want it really fizzy then just have a smaller amount more often. Let it settle down before you drink it.
I found that if I had too much, too often that it would give me diarrhea. I have read about athletes using bicarbonate of soda to improve their performance and I'm pretty sure they were using quite a lot more than me.
I found that if I had too much, too often that it would give me diarrhea. I have read about athletes using bicarbonate of soda to improve their performance and I'm pretty sure they were using quite a lot more than me.
Last edited:
WestCoaster
Member
Eliminating fructose has been the only way to stop gout for me. No word of a lie, when I start the consumption of it (unless it's fruit coming from berries), gout returns.
When i got gout for the first time, my doctor said (cut down meat), so I did, gout came back. When I went to my naturopath, he said cut down sugar, so i did, and it hasn't returned since. Baking soda in water has worked, but then I thought to myself "why must I have to dump baking soda in my water to to alleviate gout, when I simply would rather not have it in the first place". Luckily now, I am find with berries and low to moderate amounts of fruit from time to time.
At the time my Naturopath thought it was fatty liver, but it turned out after an ultrasound, there wasn't enough there to warrant being diagnosed with NAFLD.
When i got gout for the first time, my doctor said (cut down meat), so I did, gout came back. When I went to my naturopath, he said cut down sugar, so i did, and it hasn't returned since. Baking soda in water has worked, but then I thought to myself "why must I have to dump baking soda in my water to to alleviate gout, when I simply would rather not have it in the first place". Luckily now, I am find with berries and low to moderate amounts of fruit from time to time.
At the time my Naturopath thought it was fatty liver, but it turned out after an ultrasound, there wasn't enough there to warrant being diagnosed with NAFLD.
Any idea how baking soda relieves gout?
How does Ceylon cinnamon help? What's the mechanism involved?
I've read about fructose increasing uric acid but wonder why fructose would but not glucose. Does this have something to do with fructose being metabolized directly by the liver?
But if avoiding sugar (and therefore fructose) is the answer, as this reduces uric acid production, it would also make sense then to remove all food that contributes to uric acid production such as liver. Since uric acid is a very important antioxidant, that approach would deprive one of a protective substance. So, the solution has to deal more with how to keep uric acid from turning into sodium urate crystals. Seems like there is a regulatory mechanism that isn't working well.
I have had high uric acid, even above range, and it isn't causing me to have gout at all. I'm glad for it because I get that high level of uric acid because the body needed it for my high lead condition. But, I don't why I'm not having gout. Is it because my body is using that uric acid (to counter oxidative damage that might occur without it)? Or is it because a regulatory mechanism is working to keep gout from occurring? Could it be because my thyroid is working, as I have heard Ray talk about thyroid being needed to relieve or prevent arthritis? Is gout a form of arthritis? Is there a connection to carbon dioxide, as taking baking soda relieves gout, and would this lead back to thyroid, as it is an enabler of oxidative metabolism, of which carbon dioxide is a beneficial byproduct?
I also note that since I've started taking large quantities of vitamin C, I have also experienced lower uric acid levels. I would think that the level of uric acid should not be as relevant as other confounding factors in the discussion of gout.
I'm inclined to look into all the factors that affect oxidative metabolism first, starting with thyroid, but also other factors that affect the enzymatic processes entailed in enabling oxidative metabolism. Gout would easily then be a disease of metabolism, if true.
I've thought about my magnesium deficiency, as well as the associated potassium deficiency arising from it, and I'm addressing it with supplementation. But I don't understand why despite my magnesium and potassium deficiency, I haven't experienced gout. One possible explanation could be a matter of degree. Perhaps I wasn't enough deficient. Another possibility was that due to my huge antioxidant requirement (from lead toxicity), my high uric levels were being fully utilized, and thus keeping it from doing mischief.
Many factors are considered in the crystallization of monosodium urate:
The Crystallization of Monosodium Urate :
Sone of the factors:
Temperature is another environmental factor that appears to play a role in MSU crystal formation through effects on urate solubility [27–29]. In vitro studies performed in aqueous solutions suggest that a reduction of even 2 °C, from 37 to 35 °C, is sufficient to lower the solubility point of urate from 6.8 to 6.0 mg/dL [28]. This response to temperature may explain in part why the first metatarsophalangeal joint—an area of both relatively reduced perfusion (suggesting reduced heat delivery from the body core), and relatively increased surface-to-volume ratio (promoting heat radiation and loss)—is the most common site for first gouty attacks.
Like cold temperature, the presence of an acidic environment also appears to facilitate MSU crystallization. Wilcox et al. demonstrated that reduction of pH promoted MSU nucleation in an in vitro system [30]. In this model, they found that the pH directly affected the nucleation of crystals by a mechanism not well understood, but apparently independent of the MSU solubility level. In addition, pH exerted an indirect effect on MSU crystallization by increasing calcium ion concentrations that consequently reduced MSU solubility and promoted nucleation [30]. The authors therefore proposed that increased levels of free Ca++ ions in the setting of lower pH (resulting from displacement of plasma protein-bound Ca++ into the liquid phase) may explain the relationship between acidic environments and MSU nucleation. They also speculate that the initial nucleus of an MSU crystal may be a calcium urate molecule, or that, because of their nearly identical atomic radii, calcium ions may substitute for sodium in the urate crystal lattice [30]. Acidosis occurs in conditions such as strenuous exercise, respiratory insufficiency, and ethanol consumption, all of which are associated with the development of gout attacks.
Interestingly, the metabolic activity of neutrophils during phagocytosis of existing crystals may result in lactic acid generation, thus lowering the synovial fluid pH and promoting additional local impetus for crystal formation. Consistent with this model, increasing lactic acid and declining pH have been observed in the synovial fluid of acute gout (incubated in vitro at 38 °C) [31]. It has been postulated that the increased incidence of acute gouty attacks that occurs during sleep may be due in part to the mild respiratory acidosis that ensues when breathing rates decline [32].
While there are many other factors postulated, the above highlighted factors point to the possibility that gout is a disease of metabolism.
The Crystallization of Monosodium Urate :
Sone of the factors:
Temperature is another environmental factor that appears to play a role in MSU crystal formation through effects on urate solubility [27–29]. In vitro studies performed in aqueous solutions suggest that a reduction of even 2 °C, from 37 to 35 °C, is sufficient to lower the solubility point of urate from 6.8 to 6.0 mg/dL [28]. This response to temperature may explain in part why the first metatarsophalangeal joint—an area of both relatively reduced perfusion (suggesting reduced heat delivery from the body core), and relatively increased surface-to-volume ratio (promoting heat radiation and loss)—is the most common site for first gouty attacks.
Like cold temperature, the presence of an acidic environment also appears to facilitate MSU crystallization. Wilcox et al. demonstrated that reduction of pH promoted MSU nucleation in an in vitro system [30]. In this model, they found that the pH directly affected the nucleation of crystals by a mechanism not well understood, but apparently independent of the MSU solubility level. In addition, pH exerted an indirect effect on MSU crystallization by increasing calcium ion concentrations that consequently reduced MSU solubility and promoted nucleation [30]. The authors therefore proposed that increased levels of free Ca++ ions in the setting of lower pH (resulting from displacement of plasma protein-bound Ca++ into the liquid phase) may explain the relationship between acidic environments and MSU nucleation. They also speculate that the initial nucleus of an MSU crystal may be a calcium urate molecule, or that, because of their nearly identical atomic radii, calcium ions may substitute for sodium in the urate crystal lattice [30]. Acidosis occurs in conditions such as strenuous exercise, respiratory insufficiency, and ethanol consumption, all of which are associated with the development of gout attacks.
Interestingly, the metabolic activity of neutrophils during phagocytosis of existing crystals may result in lactic acid generation, thus lowering the synovial fluid pH and promoting additional local impetus for crystal formation. Consistent with this model, increasing lactic acid and declining pH have been observed in the synovial fluid of acute gout (incubated in vitro at 38 °C) [31]. It has been postulated that the increased incidence of acute gouty attacks that occurs during sleep may be due in part to the mild respiratory acidosis that ensues when breathing rates decline [32].
While there are many other factors postulated, the above highlighted factors point to the possibility that gout is a disease of metabolism.
alywest
Member
- Joined
- Apr 19, 2017
- Messages
- 1,028
Clin Exp Rheumatol. 2001 Nov-Dec;19(6):661-5.
Hyperuricemia and gout in thyroid endocrine disorders.
Giordano N, Santacroce C, Mattii G, Geraci S, Amendola A, Gennari C.
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.
obtained from functionalalps.com
The effect of mini‐dose aspirin on renal function and uric acid handling in elderly patients
******* it hurts. Never had other problems than with left big toe, now I have pain in multiple places. Quite sure it has something to do with the aspirin and other "Peaty" stuff like liver, coffee, fructose etc.
******* it hurts. Never had other problems than with left big toe, now I have pain in multiple places. Quite sure it has something to do with the aspirin and other "Peaty" stuff like liver, coffee, fructose etc.
alywest
Member
- Joined
- Apr 19, 2017
- Messages
- 1,028
Are you supplementing thyroid?
UG Krishnamurti
Member
- Joined
- Sep 28, 2020
- Messages
- 555
In my own experience I only get gout when eating some butter for a couple of days. I've experimented like 10x and It's always a few days after butter.
Ice cream is fine. Coconut oil is fine. Olive oil is fine. But butter is NOT.
Then somebody posted some study which could maybe explain some mechanism behind it which made sense to me:
jamanetwork.com
"ADEQUATE EVIDENCE is available to indicate a relationship between uric acid and lipid metabolism. Previous studies, however, have been confined to correlations between uricemia and the blood cholesterol in patients with gout or chronic hypercholesterolemia, or in other conditions where there may be an acute hyperlipidemia such as in diabetic acidosis. Preliminary findings suggesting a more precise association between the uric-acid levels and the blood triglycerides rather than the cholesterol, prompted us to investigate this more closely."
I am not sure what "lipid metabolism" is and if we should improve it but It could point to a right direction.
Increasing triglycerides/cholesterol could exacerbate gout?
Very probable in my case.
Ice cream is fine. Coconut oil is fine. Olive oil is fine. But butter is NOT.
Then somebody posted some study which could maybe explain some mechanism behind it which made sense to me:
Blood Lipid and Uric Acid Interrelationships
ADEQUATE EVIDENCE is available to indicate a relationship between uric acid and lipid metabolism. Previous studies, however, have been confined to correlations between uricemia and the blood cholesterol in patients with gout or chronic hypercholesterolemia, or in other conditions where there may...
jamanetwork.com
"ADEQUATE EVIDENCE is available to indicate a relationship between uric acid and lipid metabolism. Previous studies, however, have been confined to correlations between uricemia and the blood cholesterol in patients with gout or chronic hypercholesterolemia, or in other conditions where there may be an acute hyperlipidemia such as in diabetic acidosis. Preliminary findings suggesting a more precise association between the uric-acid levels and the blood triglycerides rather than the cholesterol, prompted us to investigate this more closely."
I am not sure what "lipid metabolism" is and if we should improve it but It could point to a right direction.
Increasing triglycerides/cholesterol could exacerbate gout?
Very probable in my case.
Did it get better?
Mito
Member
- Joined
- Dec 10, 2016
- Messages
- 2,554
The inhibitory kinetics of vitamins B9, C, E, and D3 on bovine xanthine oxidase: Gout treatment - PubMed
The obtained results promise an excellent strategy using vitamins to enhance immunity, treat hyperuricemia, and minimize the usual drug side effects.
pubmed.ncbi.nlm.nih.gov
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