Low Oxalate Diet, a possible explanation for its effectiveness

[XenMan]

My explanation on oxalate is completely different. I have discussed this with notnowdad awhile back on other forums and we agree to disagree.

I have been constantly oxalate dumping for over 2 years now starting with numerous times per day and now just at night. My RLS has improved significantly with a strong correlation with dumping. Alcohol and coffee are good catalysts for dumping and very bad nights of RLS. I can also use a TENS machine with footpads and that also leads to great dumps and more bad RLS. So my RLS hell should end when I can get the oxalate all out and then manage oxalate to make sure it doesn't return, but for now I dump twice a week with bad nights and the rest are mild symptoms that let me return to sleeping enough to feel normal again.

Oxalate in my diet makes no difference.

I'm not part of the 'iron cult' as I call it for RLS, as iron is impacted by sleep deprivation just like dopamine. Oxalate binds with iron and disrupts iron processes in the body as others have mentioned but there is a very large cohort of people with oxalate issues as well as those with autism who have high oxalate and potential iron issues; but not high rates of RLS. So iron then becomes 'if susceptible', with all the other successful non iron treatments, as well as physical causes of RLS contradicting low iron as 'the cause', so the mental gymnastics for the iron cultists become bizarre or they are just hostile like most people online who can't accept opposing views.

So RLS seems to be purely neurological for some as part of a brain change with motor and sensory functions reacting to normal signals. But also for many such as venous insufficiency, nerve entrapment, after knee operations, MCAS and anecdotally fascia issues, RLS is a motor and sensory reaction to something physical. So maybe iron plays a part for the purely neurological and not for others.

My RLS is definitely physical as I can locate and treat the trigger points. These trigger points are created by oxalate dumping, or if you haven't cleared your kidneys enough for dumping it is from what I call 'oxalate modulation' as oxalate is moved to balance from storage, blood level and absorption from food. If dietary oxalate changes helps then you should investigate physical trigger points, and if you have physical trigger points or physical treatments make your RLS better of worse, then explore oxalate.

It is possible that some have non physical, purely neurological RLS from oxalate if low iron triggers a motor and sensory response, but forums are full of people who have tunnel vision and rigid view that everything has to be just one thing. RLS is best seen as a symptom, and oxalate may lead to numerous situations or conditions that create RLS symptoms.

[Frunobulax]

It is possible that some have non physical, purely neurological RLS from oxalate if low iron triggers a motor and sensory response, but forums are full of people who have tunnel vision and rigid view that everything has to be just one thing. RLS is best seen as a symptom, and oxalate may lead to numerous situations or conditions that create RLS symptoms.

I agree. Medicine tends to home in on "the one". Even in diabetes, perhaps the most researched disease ever, 100 years after discovering insulin, most doctors still don't understand that there are very different mechanisms leading to the high blood sugar (type 1/type 2), and that treatment must differ even if the symptoms are (nearly) identical. In fact, what's life saving for one (insulin for T1D) worsens the disease for the others (T2D), at least in the early stages. (In the late stages of T2D the pancreas might be gone and unable to produce any insulin, those patients will also need insulin. But there are studies showing that this affects less than half even of the patients that had to take diabetes drugs for many years.)

There is no "the one" cause for RLS, or at least I would be extremely surprised if there were one. Chances are we have very many different root causes and possibly very different pathomechanisms leading to the symptoms. What I posted in this thread is to be considered a mechanism that could cause RLS symptoms, for a fraction of RLS patients where we have no idea if it's closer to 0% (or actually 0% because the theory is bs) or 100%. Oxalates are little researched because of tunnel vision on kidney stones, but we do know that oxalate crystals can form all over the body. Clearly oxalate has no problem to pass the blood brain barrier, either. Symptoms vary a lot among people who have identified oxalates as issue, but often it's not clear if oxalates are the root cause or just one of many factors.

It seems clear to me that there are different types of RLS: Some people describe it as painful, others not as painful at all. You describe trigger points, while for me RLS is a whole body experience -- symptoms often start with a weird feeling of tension all over my body, before I get the urge to move body parts, but there is no local treatment that works for me.

So it's no stretch of imagination that there may be very different root causes for RLS. But this doesn't rule out that there are common (or at least dominant) pathomechanisms for our symptoms. (Yeah, medicine often doesn't distinguish between root causes and symptoms. I believe it makes all the difference in the world.) Now, I see basically 2 possibilities.

• There is a unifying mechanism that causes RLS symptoms. In this case, iron metabolism would be a good place to start, even if it doesn't affect all RLS sufferers.
• Or, there is no unifying mechanism and the different types of RLS symptoms correspond with different pathomechanisms. We could have dozens of root causes and maybe as many ways how RLS symptoms are caused. And this is the scenario that appears more likely to me. Which implies that whenever we talk about pathomechanisms, we must understand that we're talking only about a part (and possibly a small one) of RLS patients. And also implies that we need personalized medicine/treatment. Still, for every individual there is a clear causal chain going from root cause to symptom, and understanding these chains is our only hope.

But as to iron... I don't think it's wrong to do a lot of research there, and I still find the oxalate/iron connection very intriguing. If about 60% of RLS patients respond well to iron infusions (or what was the latest number), then iron clearly plays a role in RLS. Now some of them may simply suffer from iron deficiency, for others it might be that a very high concentration of iron compensates for some other issues. (If I may digress a bit: This is known from other trace minerals, for example there is a small study that some fibromyalgia patients improve significantly if they take huge doses of vitamin B1, like 2-3 grams a day. The conjectured reason is that B1 transport into the cells is broken somehow, but if you create a high enough plasma concentration then some B1 will diffuse into the cells anyway.)

Then there is the conjecture that started the thread, that oxalates may impede iron transport by binding to transferrin. This could affect part of the other 40%: There is no serum/ferritin deficiency but a "functional" deficiency, that iron is not released where it's needed -- and an iron infusion will not help, because it will only add to the serum/ferritin iron.

So focusing on the role of iron should give us insight into the pathomechanisms for at least 60% of us, shouldn't it? (Even if I may not be among them, because iron IVs did nothing for me.)

[Oozz]

So focusing on the role of iron should give us insight into the pathomechanisms for at least 60% of us, shouldn't it? (Even if I may not be among them, because iron IVs did nothing for me.)

What type of iron formulation? What was the protocol? How long did you wait to assess symptoms?

[XenMan]

[*] There is a unifying mechanism that causes RLS symptoms. In this case, iron metabolism would be a good place to start, even if it doesn't affect all RLS sufferers.

There are so many papers on iron that contradict each other, I stand as I always have that iron is good as of one the many treatments but overall is a nothingburger for the cause of RLS. If it was you would see other impacts from this iron metabolism issue. There are so many claims on forums about RLS from 'this and that' where the only symptom is RLS. This is kinda silly.

I'm still open to low iron and iron metabolism issues being one of the numerous conditions that causes the RLS process to start. But too many are heavily invested in it, and it is irresponsible for some the leading hospitals and doctors on RLS to be promoting iron as the cause.

[Frunobulax]

[*] There is a unifying mechanism that causes RLS symptoms. In this case, iron metabolism would be a good place to start, even if it doesn't affect all RLS sufferers.

There are so many papers on iron that contradict each other, I stand as I always have that iron is good as of one the many treatments but overall is a nothingburger for the cause of RLS. If it was you would see other impacts from this iron metabolism issue.

That's why I consider this option the less likely one of the two Usually contradictory papers mean that the researchers failed to control for a major influence, some factor that's usually more important to the disease than whatever they're studying. Like, for example, treating N different diseases as one, and trying to treat all of them with the same drugs because they have similar symptoms, even though the correct treatment is very different depending on the disease. (But that's me conjecturing again.)

Still, contradictory paper are usually a good start if (if!) you try to figure out why they contradict each other. Another thing that is very rarely done in medical literature, somehow scientists believe that if you have 20 papers claiming something and 25 claiming the opposite, then the problem can be solved by doing another 20 studies. (Or sometimes there is some financial involvement from some third party. Between the 60s and 80s, IIRC, whenever a paper would call out trans fats for being dangerous, half a year later 5 papers would be published claiming the opposite, papers mysteriously sponsored by the margarine industry. Ah well.)

[XenMan]

Usually contradictory papers mean that the researchers failed to control for a major influence, some factor that's usually more important to the disease than whatever they're studying.

I think this or a few more comments will be my final involvement in any of RLS forums online because RLS based on the diagnosis criteria is just an urge to move the legs which includes so many conditions as well as mental health issues and purely physical. This is why all the iron research is contradictory and almost all RLS research is becoming useless. Most people who appear on RLS forums do not have WED RLS, they have akathisia, neuropathy or for fun Google all conditions with 'restlessness' as part of the symptoms.

I could create a flowchart to better identify conditions, but RLS has become a cult with the forces of evil winning so anyone who suggests good reasons for anything different is insulted and excluded. So the future is lots of bad drugs with bad side effects and bad outcomes for many who don't really need it.

If I still had RLS as the major issue it was a few years back I would be frustrated and angry. But since I sleep well these days I'm just disappointed and feel sorry for those who don't get relief.

[SquirmingSusan]

Frunobulax, have you found the alanine to be helpful? This is all very interesting, but not doable for me because just about everything I can still eat is high oxalate. I do take calcium and magnesium, zinc, and B vitamins. But I'll try anything to find out if it helps.

[Frunobulax]

Frunobulax, have you found the alanine to be helpful? This is all very interesting, but not doable for me because just about everything I can still eat is high oxalate. I do take calcium and magnesium, zinc, and B vitamins. But I'll try anything to find out if it helps.

This question is a tough one I can't say that my RLS has changed in overall severety, but it's under control with 20mg Oxycodone a day. But my main condition is ME/CFS, and I had a pretty good summer compared to the years before. So maybe the alanine does something after all.

But my RLS has changed somewhat in the last 6 months. It seems I'm now ultra sensitive to alcohol -- I used to tolerate 2-3 glasses of wine in the evening without a worsening of symptoms, while now it seems that any amount of alcohol triggers RLS. Also my symptoms, if they occur, tend to manifest once more during the evening before I take my night dose of Oxy, a more traditional pattern. (I used to be pretty symptom free in the evening, but my RLS breakthroughs would occur in the early morning, after 4-5 hours of sleep.)

I'm still taking the beta alanine, but I'll probably stop it once I run out and see if it makes a difference.

[SquirmingSusan]

This question is a tough one I can't say that my RLS has changed in overall severety, but it's under control with 20mg Oxycodone a day. But my main condition is ME/CFS, and I had a pretty good summer compared to the years before. So maybe the alanine does something after all.

Thanks for answering. Seems like alanine works similarly to creatine, in that they both help the body restore muscle. I might give it a try. I do that my iron runs low because of gastric bypass, and my RLS gets much worse when my ferritin is low. I'm in the middle of a series of iron infusions and am looking forward to some relief from that.

Have you looked into L-citrulline malate for the CFS? It's supposed to be helpful for fibro, so that might be worth a try. It converts to arginine in the body, and many people find it helpful for overall energy. It didn't do much for me, but other people who have narcolepsy have had some success. I get better results just taking arginine, but get sick of taking stuff all the time.

[Frunobulax]

Have you looked into L-citrulline malate for the CFS? I

I have tried pretty much any supplement ever mentioned under the sun From reading a lot of literature and discussion a lot with other patients, the one thing I'm sure of is that ME/CFS is not one illness, but a symptom group that can be caused by a multitude of issues. Symptoms vary greatly (apart from the one unifying symptom PEM, post excertional malaise) and it seems that pretty much all supplements (with a few notable exceptions, mostly antioxidants) help a few patients but worsen the symptoms for others.

Back to oxalates... I'm positive that oxalates do contribute to my RLS. There is a general sense that I'm doing better since greatly reducing oxalates (I could reduce the dose of oxycodone), but I also had a rather controlled experiment (though n=1) that proves this, in my opinion: I have regular stays in a clinic that treats ME/CFS, where I was 7 times (3 weeks each), and I kept exactly the same diet plan for the last 6 times. (When I was there for the first time I still ate carbs, but I was low carb for the last 6 stays.) Now this is a clinic that puts a lot of emphasis on that nutrition is a key component of the treatment, so you're not allowed to eat anything except what they prepare, or exceptions greenlit by their nutritionist. Since I adhered to that, I can say that I know exactly what I ate in those 6 times 3 weeks. (They follow a rotational plan without any variation.) Out of these 6 stays, during the first 3 times my RLS would go through the roof after about 7-10 days. Then I learned about oxalates and eliminated the foods with the highest oxalate content (spinach, almonds and beetroots), and for the last 3 times I was there, my RLS was perfectly fine.

But since a strict low-oxalate diet does not improve/eliminate my RLS further, it seems there are other contributing factors.