I’m often touch and go on this forum and make lots of typos. I meant to write, “over-hydrating.” He said adding a bit of lemon juice to my water jug would also speed up the dissolution process. Otherwise there’s a commercial solution which if memory serves was some sort of citrate salt. Maybe potassium citrate? He said a dash of lemon juice is just as effective.
And if all fails, since my stones seemed to be oxalate based, the next step would be shockwave therapy. That would make them crumble. I haven’t been back for a checkup especially since I’d need a CAT scan with contrast and I’m not particularly keen on getting the radiation. My stones haven’t moved at all so they don’t bother me and have been out of sight out of mind for the most part. I’ve got a lingering low grade bladder infection (basically a chronic UTI) that’s really been raining on my parade so I’m determined to fix up my whole UTI system but unfortunately all the things I’ve recently learned are inapplicable during pregnancy so I have to wait a few months.
Basically for kidney stones, especially when they’re not huge, there’s plenty of research showing natural compounds can help break them up. I haven’t bookmarked the literature but it is extant in pubmed. And there are commercial products on Amazon— basically kidney stone supplements — containing those research backed ingredients that the reviewers rave by.
So I do think there’a better modalities besides over hydration and short of shockwave therapy.
I have seen many cases where there are those with dangerously low sodium levels (129 - 131) with extemely high blood pressures. In that case how would you quickly restore the sodium levels, without increasing the bp is the dilemma. Usually it is a renin and aldosterone problem in the kidney, not so much diet. But nevertheless sodium is extremely tricky.
For example, It should slowly be ingested or IV’d (and diluted!!!) and in balance with other minerals. I think the problem is eating or drinking sodium rich items without dilution. Like an extremely salty snack or drink where you get all the sodium in one shot instead of diluting it and drinking it throughout the day in small amounts. I think peter attia said it somewhere, that that exact dilution problem could be the reason for such contradictory and opposing studies on the benefit and harm of sodium.
Citric acid (lemon juice) has the disadvantage of being acidic. The other citrates are alkaline. Hence taking more of the others should be ok. But i would be careful taking a megadose in pregnancy. It is unpredictable. (As to the question as to how much is a megadose, I have taken 70g in a day - as a test - not recommended - and am currently taking 15g a day, but I would think under 2g would be outside the large doses territory. There is perhaps 3g in a single lemon which is mainly citrate.)
Incidentally eating lemons to get increased acetylation has a difficulty in that you are eating acid. When cells get acidic they deacetylate the histone to get back to mildly alkaline. Hence eating lots of lemons is not something I would advise.
Best to go to the right thread for this. The question as to what quantities to take when and in what mix is sadly really quite complicated although to some extent you can try things and see what happens. The balance between the 4 cations does matter.
They seem to increase serum sodium.
I wouldn’t use drugs for this, it seems risky to mess with kidney / water / sodium balance unless you’ve read a lot on the drugs you want to use and monitor it.
As far as I understand it, it is hard to mess with your sodium levels so they go too low with diet if you are healthy and not using drugs, and not doing long exercise sessions where you overhydrate.
Doctors might be neurotic about eating sodium since they see patients on polypharmacy, unhealthy, probably metabolic syndrome, with hyponatremia.
It doesn’t make any sense that it would be a diet problem causing such conflicting results, by extremely increasing BP, with hyponatremia, as the Yanomani indians had low BP (100~) throughout their lives asymptomatic. My BP has slightly been trending downwards ever since I started low sodium diet (again). I also doubt most people are able to get to an extremely low sodium diet, especially people who are unhealthy in general and on polypharmacy.
The reason for contradictory results is confounding, simply.
But I the dilution aspect of things is interesting.
In fact looking at my records my peak day for supplementing with Citrate was 75g of Citrate. That is perhaps 50g of Citrate with Sodium which means likelihood is about 15g of Sodium in the form of Sodium Citrate (without doing precise calculations).
My night time BP-HR after this was a bit high at 130/76-52, but morning it dropped to 119/71-52
The next day I had 40g citrate so perhaps around 8g sodium, but I had had a drink (or n) of alcohol so my night time BP-HR was 110/62-54.
@AnUser Thanks. For context cana is very attractive to me based on a wealth human mortality and disease data and the ITP longevity results and mechanistic rationales. So it would not be because of the sodium effects Per Se
None, sorry. Here’s what I’ve just found after a quick research:
SGLT2 inhibitors, sodium and off-target effects: an overview 2020: “Actually, sodium and water depletion may contribute to some positive actions of SGLT2i but evidence is far from being conclusive and the real physiologic effects of SGLT2i on sodium remain largely unknown. Indeed, no study has yet investigated how SGLT2i change sodium balance in the long term and especially the pathways through which the natriuretic effect is expressed.”
Metabolic Communication by SGLT2 Inhibition 2023: “SGLT2i reduced microbiome formation of uremic toxins such as p-cresol sulfate and thereby their body exposure and need for renal detoxification, which, combined with direct kidney effects of SGLT2i, including less proximal tubule glucotoxicity and a broad downregulation of apical transporters (including sodium, amino acid, and urate uptake), provides a metabolic foundation for kidney and cardiovascular protection. […] SGLT2i reduce the early proximal tubule uptake not only of sodium and sugar but of many other metabolites, which decreases cardiovascular risk factors such as hypertension, volume retention, and hyperuricemia.”
It seems to me from below that the effect is likely to go in the other direction - that they are lowering sodium in the body similar to how they lower sugar levels?
Hydration is probably the key, and low sodium helps with that but might not be necessary. It would be very nice if that is not the case, which might be so. I do suspect that hydration removes many side effects of sodium.
@AnUser do you have any more color on your statement above?
I spent more time trying to look at it and it really seems to be the opposite to me - but since you said it so matter of fact I want to double check if I’m missing something?
We have the papers that @adssx shared and that @AlexKChen usually seems to be correct when he says something asa fact
The very name suggests it - it even has sodium before it has glucose…. Sodium-glucose cotransporter inhibitor/inhibition (SGLTi)
Here is how Peter Attia described it:
The other important question here is, *Are there other benefits associated with be it Canagliflozin or other SGLT2 inhibitors that go beyond the glycemic control? *
In addition to weight loss, we’re also seeing a greater reduction in blood pressure
Why might this happen? ⇒ when you block SGLT2, you’re preventing the kidney from reabsorbing not just glucose but sodium
As a patient is excreting more glucose and sodium in their urine, you would think they have obviously less sodium within their plasma.
That may explain the benefits we see on the blood pressure front as well
Seems that it did not increase sodium in healthy volunteers, and only perhaps in this specific group suffering from low sodium levels
Currently, there are relatively few studies on SGLT 2i and hyponatremia, and little clinical evidence of significant serum Na+ elevation with SGLT 2i. However, based on the studies previously discussed in this paper, particularly the double-blind placebo-controlled trial by Refardt (Refardt et al., 2020), SGLT 2i may be a viable new treatment for hyponatremia, but its efficacy and safety need further confirmation. The following section provides a brief summary of the potential mechanisms by which SGLT 2i restores the sodium balance in patients with hyponatremia.
So this seems more in line with restoring sodium balance in a specific sodium related disease population than increasing it across the board or in healthy individuals