Another year of relief (Low-oxalate diet)

[Frunobulax]

Is your diet very salty? Maybe you are not potassium deficient, but your balance between sodium and potassium is bad? Furthermore oxalic acid likes to react with potassium and other minerals to form oxalate salts. Maybe the vegetables that you eat are high in oxalic acid, which reacts with the potassium?

I don't add salt to anything, so I doubt it's that. I do eat veg's that are high in oxalic acid, but so do a lot of people.... Anyway, I will continue to think about it. Maybe I will ask my doc if I can get it tested next time I see her.

Low salt intake may lead to potassium deficiency (read https://www.virtahealth.com/blog/sodium ... l-function, it's a more general article about salt). Furthermore, potassium deficiency shows up very late in bloodwork as the body tries to maintain the potassium level in the blood at all cost. If your blood shows low potassium levels then you're probably experiencing severe symptoms, but the reverse is not true: If your potassium levels are OK then you may still be deficient.

[Deb212]

Three plus months on a low oxalate eating plan. I have occasional RLS that can be walked off. RLS no longer prevents me from sleeping or enjoying sedentary activities. I have no idea why, it just is.

I'm not looking for why or how. I've been making myself crazy for over 40 years trying to figure it out and never found a solution.

It took awhile but I've been able to figure out what I can eat and I have a very varied diet of plant based foods that do not seem to make my RLS worse so I'm not afraid of not getting nutrients from the food I eat. I'm way more afraid of the augmentation that almost caused me to take my own life. There are lots of great groups that can help with low oxalate eating and I would encourage anyone wanting to try it to look them up.

One thing that really, really helped was Jim's information about how the offending food shows up 24 hours later. I was always looking at a closer correlation between eating something and symptoms but have (through a food chart) seen it is 24 hours or the next night almost always. Please know I appreciate all your information and that you are sharing your ideas.

Praying for everyone to find peace.

Deb

[ViewsAskew]

Three plus months on a low oxalate eating plan. I have occasional RLS that can be walked off. RLS no longer prevents me from sleeping or enjoying sedentary activities. I have no idea why, it just is.

I'm not looking for why or how. I've been making myself crazy for over 40 years trying to figure it out and never found a solution.

It took awhile but I've been able to figure out what I can eat and I have a very varied diet of plant based foods that do not seem to make my RLS worse so I'm not afraid of not getting nutrients from the food I eat. I'm way more afraid of the augmentation that almost caused me to take my own life. There are lots of great groups that can help with low oxalate eating and I would encourage anyone wanting to try it to look them up.

One thing that really, really helped was Jim's information about how the offending food shows up 24 hours later. I was always looking at a closer correlation between eating something and symptoms but have (through a food chart) seen it is 24 hours or the next night almost always. Please know I appreciate all your information and that you are sharing your ideas.

Praying for everyone to find peace.

Deb

So awesome!

[badnights]

Low salt intake may lead to potassium deficiency (read https://www.virtahealth.com/blog/sodium ... l-function, it's a more general article about salt). Furthermore, potassium deficiency shows up very late in bloodwork as the body tries to maintain the potassium level in the blood at all cost. If your blood shows low potassium levels then you're probably experiencing severe symptoms, but the reverse is not true: If your potassium levels are OK then you may still be deficient.

Wow - - there's so much to learn. (Or maybe I'm excited because I feel like I have a brain again since I stopped zopiclone).

I think, from the link you sent, that the problem of low salt intake leading to K deficiency is only for people in ketosis - which I am not (though I don't eat a whole lot of carbs). That said, it sounds like no one has actually studied low-salt diets, so it might be true for others as well.

It seems that a tissue mineral analysis (TMA) on a hair is more sensitive than blood tests for detecting potassium deficiency. Also, other minerals besides potassium are assayed, so ratios can be calculated that reveal imbalances - too much calcium relative to potassium, for example, which might (depending on circumstances) be corrected better by lowering calcium intake than increasing potassium intake. I wonder if I could convince my doctor that I needed a TMA....

the offending food shows up 24 hours later. I was always looking at a closer correlation between eating something and symptoms but have (through a food chart) seen it is 24 hours or the next night almost always.

I am going to be kicking my own butt really hard if I eventually try this diet and it helps significantly, as it seems to for those who have tried it seriously. This advice is some that I'll have to remember.

[EVogel]

6. Myo Fascial Release. The most god awful miserable massage you'll ever get. They belive RLS is a fascia issue...energy is trying to move but it is blocked by folds of fascia. I had three treatments. One he worked on my feet. The next, my bladder, his fists buried into my gut. But ever since I amhttp://bb.rls.org/index.php urinating less frequently day and night than I have for ten years. Remember, my RLS included 6-8 trips to the bathroom every evening. https://www.myofascialrelease.com You can find a practitioner in your town if you choose. I am continuing these weekly.

Oddly, he was drawn right to the spot where my ingral hernia surgery was, several months earlier, also near by bladder, which was extremely tender and bunched up, and right in front of the sacrum, where I've always felt the restlessness "originating." Remember, my RLS kicked in big time after the h surgery. So why exactly did I have the hernia? There is only one piece of fascia running through your entire body and it gets bunched up like cellophane, preventing cell to cell communication, the release of waste, nutrient absorption, etc.

Thanks so much for sharing all your experiences, trials and tribulations. Like you ja trying the low oxalate diet, yoga ( stretching exercises) and the myofacial release theraphy. It has been a couple weeks and my legs are not as desperate every night. I still take long baths or shower at night but I am able to relax more at night.

Ditto for your words below:

Lord have mercy. Those were some tough months this past winter. Such desperation and despair. It's hard for me to even visit this website.

Thanks for expressing some of the feelings that I could not put in words, but you did so eloquently.

Ellie

[Frunobulax]

I think, from the link you sent, that the problem of low salt intake leading to K deficiency is only for people in ketosis - which I am not (though I don't eat a whole lot of carbs). That said, it sounds like no one has actually studied low-salt diets, so it might be true for others as well.

Saw this a bit late, sorry...
I think the mechanism is a bit different. Most people on keto choose this diet because they were severely overweight and struggle with health issues like hypertension. They have been told by their doctors to avoid salt, so they will avoid salt. Then they go on keto, their kidneys recover, and suddenly they don't get enough salt because they are so used in using little or no salt... I think people would be OK if they would salt to taste, but might run into problems if they try to stick to low salt.

Our evolution has set us up in a way that we can overeat most of the essential electrolytes and micronutrients, and the body will simply excrete the excess stuff. (This is the only way how the body can safely maintain the required amount of electrolytes.) Now enter a life of high carb&sugar food and insulin resistance, and suddenly we get a big problem if we eat too much salt: A frequent problem for patients with high insulin (=85% of the adult western population) is that kidneys have a reduced efficiency, so they can't clear the body from excess salt and other electrolytes. There is some truth that salt leads to high blood pressure, but the main mechanism is not the overeating of salt but the impaired kidney function. Studies show that radical salt reduction will only improve hypertension by a tiny amount, yet the urban myth that salt intake leads to hypertension does not die. (I could dig out the references for that if you like.)

So my personal advice (disclaimer: I'm not a doctor) would be this: Salt to taste, eat as much salt as you like, unless you have major known kidney issues. And if you run into problems with hypertension or too much water, then reduce the amount of carbs in your diet. If you have no issues with hypertension or water, then the amount of carbs is probably OK. (HbA1c should be below 5.5, better at or below 5.0, this is another good measure that your carb intake is OK.)

[notnowdad]

A summary of what my experience and research have led me to believe about RLS:
1) RLS is a symptom of the body’s failure to properly handle iron distribution within the body. Iron distribution is impaired when oxalate replaces carbonate as the binding agent which attaches iron to transferrin, the body’s iron distribution vehicle. Oxalate as the binding agent “locks up” the iron and distribution is significantly impaired.
2) People who suffer from RLS tend to produce excessive amounts of the waste product oxalic acid in their livers due to a malfunction of the Citric Acid Cycle (aka Krebs Cycle). This is a non-lethal form of hyperoxaluria.
3) Limiting dietary oxalate consumption can help mitigate the toxic effects of excessive endogenous production of oxalic acid and help relieve the discomforts of RLS.
4) Achieving relief through a low oxalate diet is made difficult by the currently standard practice of spraying fresh vegetables and fruits with oxalic acid solution in order “to preserve freshness and nutrients” prior to their arrival at grocery stores. Organic vegetables and fruits are not so sprayed.
5) Eating gelatin or gelatinous soups and stews made with meat can contribute to the problem of a malfunctioning liver producing excessive amounts of oxalic acid. Glycine and vitamin C supplements can also exacerbate this problem.
6) Damage to the mucosal lining of the colon leads to excessive absorption of oxalate from food. This damage occurs when the bile, which facilitates absorption of fats in the small intestine, is not properly reabsorbed in the small intestine and enters the colon and damages the mucosal lining. Refined, bleached and deodorized cooking oils made from seeds (corn, soy, canola, etc.) are poorly absorbed in the small intestine and exacerbate this problem by carrying bile into the colon. Reuse and reheating of these oils over many days in commercial frying operations probably makes them more difficult to absorb during digestion.
7) The over production of oxalic acid by the liver is probably due to the toxic effects of dietary fluoride in public water supplies, commercially prepared beverages, tea, wine, pesticides, medicines, can liners and non-stick cookware. Dietary fluoride also impairs iron absorption from foods and this contributes to the iron utilization problems which cause RLS.
After several years of avoiding dietary exposure to both fluoride and refined, bleached and deodorized cooking oils made from seeds I seem to have recovered my ability to tolerate large amounts of dietary oxalate without experiencing RLS. I seem to be cured.

[Frunobulax]

I agree that this is one possible pathogenesis. If we assume that an iron deficit is responsible, other possible causes are an iron deficit (accounting for the 50% of sufferers that get relief from an iron IV) and other impairments of iron transport than oxalates.

I'm convinced that oxalates aren't the only factor. My RLS worsens if I consume more dietary oxalates, but I did not get any relief from an iron IV, I've been moderate oxalate (<200mg/d) for 3 years and I went to low oxalate (<50mg/d) 6 months ago and my RLS has not changed in any way. It's possible that I produce more oxalate endogenously than others, but I don't know any reliable research that would allow me to test/verify this.

Is there any research supporting your claim (2)? Which malfunctions of the citric acid cycle would cause overproduction of oxalic acid and why?

[notnowdad]

When the Covid lockdown started I used the opportunity of no longer going to restaurants to avoid the refined, bleached and deodorized cooking oils made from seeds. After a while I was pleasantly surprised to notice that my very severe allergies (seasonal pollens, dust mites and chiggers) had all vanished. After nearly a year of being allergy free, the allergies returned. It took me months to realize the relief required not only filtering fluoride from my city water, but I also had to avoid non-stick cookware (and perhaps all canned foods and drinks) that has fluorocarbons in it while simultaneously avoiding the RBD seed oils. At the beginning of the lockdown I had been experimenting with ceramic non-stick cookware which is both PFOA and PTFE free, but later I went back to using some that was only PFOA free until I realized that was a mistake. As I said above, after several years of adhering to the stricter regimen I seem to have almost fully recovered my ability to tolerate normal amounts of dietary oxalate without having RLS.

My earlier discovery that magnesium glycinate supplements triggered my RLS, led me to realize that glycine rich gelatinous meat based soups and stews did also. It was years before I started seeing on the medical websites for low oxalate diets that scientists had confirmed eating gelatin raises urinary oxalate. So far I haven’t found any research addressing my observations which suggest that glycine may be the causative factor. I mention the Citric Acid Cycle, which has oxalic acid as a waste product, in the hope that the scientists will start “picking up what I’m laying down”. The fact that they know that taking vitamin C raises urinary oxalate seems to me to suggest a plausible link to the citric acid cycle.

Both primary and secondary hyperoxaluria are considered fatal afflictions. My experience causes me to propose the potential for a third classification which is a non-lethal over production of oxalic acid. There is hard science which explains that replacing carbonate with oxalate in the binding of iron to transferrin causes the iron to get “locked up”. The only substantiation I have found concerning a connection between fluoride and hyperoxaluria is in a chapter titled “Nonneoplastic Diseases of the Kidney” by M.D. Shahrier Amin, Stephen M. Bonsib in Urologic Surgical Pathology (Fourth Edition), 2020, in a section sub-titled “Oxalate-Associated Renal Disease” it says that secondary hyperoxaluria may result from methoxyflurane anesthesia and offers the following explanation: The free fluoride in methoxyflurane appears to stimulate excessive oxalate production by the liver

A few final thoughts: I believe tea is naturally high in fluoride and many people drink it in large quantities these days. I have been avoiding American wines because of the likelihood of fluoride in the pesticides that are widely used here. I have read that many of our most common medicines, including statins, Pramipexole and many others, contain fluoride. The federal government compiles figures on our likely total exposure to fluoride and they include the disinfectants used to clean food storage facilities. I advise against using collagen supplements because of the high glycine content.

[Frunobulax]

Vitamin C does convert to oxalic acid in vitro, but I don't see the connection to the TCA cycle I'm afraid. In real life some oxalate sufferers can tolerate high doses of vitamin C while others can't (case reports from low oxalate groups), and it is unclear why we behave so differently. Same for glycine, some people seem to convert it to oxalate while others don't. In any case glyoxalate can convert to glycine, these are (to my knowledge) equilibrium states and it's not clear why one direction (glycone to glyoxalate to oxalate) may be favored for some people. Lack of vitamin B1 has been suggested but supplementation doesn't seem to help for most people.

As for processed foods, they drive chronic inflammation via high content of sugars and seed oils, among others. Inflammation impairs iron transport, driving the iron into ferritin, and pretty much all chronic inflammatory diseases may worsen or even cause RLS. While I do think it's a good idea to avoid fluoride, I don't see fluoride as a driving factor there.

Just saying we should be careful to draw conclusions from a n=1 experiment. What you write are conjectures that are in some places not backed up by research. Doesn't mean that they are wrong, but they should be clearly marked as conjectures. These are complex processes with hundreds of biochemical compounds involved and it's always tempting but usually not a good idea to focus on one substance like fluoride. Personally, all I know is that I don't know enough to form an opinion here and that we urgently need more research.

[Rustsmith]

I agree that potassium tends to taste bad. I lost my sense of smell, so the metallic taste of potassium turns me off. Sodium on the other hand tends to enhance the flavor of food. I also agree that the negative effects of sodium were overplayed and dieticians still haven't adopted the results of the latest medical research that indicate that only a small percentage of the population are susceptible to elevated blood pressure due to higher levels of sodium in their diet. They also pointedly ignore the fact that another small percentage of the population who are carriers of the cystic fibrosis gene tend to lose too much sodium in their perspiration and are therefore at risk of having their sodium levels fall too low (which is also life threatening and extremely unpleasant). You don't have to have CF, just be a carrier. In fact, before DNA testing became commonplace, the test for new parents who had a family history of CF was a skin test where a chemical was applied to induce sweating and the sweat was collected and analyzed for sodium.

I am a runner and was diagnosed after a race with a serum sodium level that was so low that it was clinically significant and just above the point where I would have been rushed to the ER for a salt solution infusion and an overnight stay. I had a horrible headache and severe nausea. Most runners in this condition get there because they drink too much water (the kidneys remove salt along with the water during the race because too much water is more dangerous to the brain, which leaves low serum sodium levels. In my case, I was both dehydrated and hyponatremic. Out of over 2000 participants in the clinical trial that I was involved with, only 4 of us had both. I later asked the doctor in charge of the trial why my situation is so rare and why they don't see that occur more often to long distance runners. Her reply was that the symptoms are so unpleasant that most quit running. But I was too goal driven and hard headed to quit, so I started taking salt pills during races to avoid future problems. When I was tested in later races, my sodium levels were in the normal range even though I had consumed around 2gm of sodium over about 4 hrs. I will also add that my BP has always been on the low side (I have fainted on several occasions) and a reading of 100/80 is high for me. As the saying goes when it comes to consuming large quantities of salt, "don't try this at home". I did so at the direction of a doctor and was checked regularly, just like we all are supposed to have our ferritin levels checked.