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Paul McGlothin

oxalates: are they a problem for calorie restrictors?

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In response to my encouragement of caution when consuming high oxalate foods, Ann, one of the Society's facebook members, asked "What do Oxalates do?"

 

I wish someone somewhere could definitively answer that question. Some who follow low oxalate diets would say that oxalates are a “junk” molecule, contained in many foods: plants, nut, beans, tea, chocolate, etc. – very deleterious to health. In fact, one group I belong to advocates a very low oxalate diet, but which is full of questionable high GI, high fat, and high protein foods – not a solution for CR folk.

 

 

Another view is that oxalates play an important role in binding with calcium and removing it from the body. It would be great if that were an efficient, well understood process. However, calcium oxalate can accumulate in kidneys to form stones as well as in other tissues. The reasons why are yet to be fully understood.

 

 

Recently a kidney expert on a livingthecrway teleconference told us about a patient who decided to eat handfuls of high oxalate nuts all day long. It caused oxalate deposits throughout his kidneys, as well as on the outside of the kidneys and on other organs— a death sentence!

 

 

Further, kidney stones are an emerging problem -- rapidly increasing in many parts of the world, especially among young women.

 

 

A problem among calorie restrictors is that many of our food selections are high in oxalates – sweet potatoes, walnuts , etc. Not only might that make oxalate deposits in tissues more likely, it might make CR folk more susceptible to pathogens.Take a look at this related study, for example:

 

 

 

Oxalate toxicity in renal cells.

> > Jonassen JA, Kohjimoto Y, Scheid CR, Schmidt M.

> > Source

> > Department of Physiology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. Julie.Jonassen@

 

 

 

Urol Res. 2005 Nov;33(5):329-39. Epub 2005 Nov 13.

> >

> > Abstract

> > Exposure to oxalate, a constituent of the most common form of kidney stones, generates toxic responses in renal epithelial cells, including altered membrane surface properties and cellular lipids, changes in gene expression, disruption of mitochondrial function, formation of reactive oxygen species and decreased cell viability.

 

 

 

Oxalate exposure activates phospholipase A2 (PLA2), which increases two lipid signaling molecules, arachidonic acid and lysophosphatidylcholine (Lyso-PC). PLA2 inhibition blocks, whereas exogenous Lyso-PC or arachidonic acid reproduce many of the effects of oxalate on mitochondrial function, gene expression and cell viability, suggesting that PLA2 activation plays a role in mediating oxalate toxicity.

 

 

 

Oxalate exposure also elicits potentially adaptive or protective changes that increase expression of proteins that may prevent crystal formation or attachment. Additional adaptive responses may facilitate removal and replacement of dead or damaged cells.

 

 

 

The presence of different inflammatory cells and molecules in the kidneys of rats with hyperoxaluria and in stone patients suggests that inflammatory responses play roles in stone disease. Renal epithelial cells can synthesize a variety of cytokines, chemoattractants and other molecules with the potential to interface with inflammatory cells; moreover, oxalate exposure increases the synthesis of these molecules.

 

 

The present studies demonstrate that oxalate exposure upregulates cyclooxygenase-2, which catalyzes the rate-limiting step in the synthesis of prostanoids, compounds derived from arachidonic acid that can modify crystal binding and may also influence inflammation. In addition, renal cell oxalate exposure promotes rapid degradation of IkappaBalpha, an endogenous inhibitor of the NF-kappaB transcription factor.

 

 

 

A similar response is observed following renal cell exposure to lipopolysaccharide (LPS), a bacterial cell wall component that activates toll-like receptor 4 (TLR4). While TLRs are primarily associated with immune cells, they are also found on many other cell types, including renal epithelial cells, suggesting that TLR signaling could directly impact renal function. Prior exposure of renal epithelial cells to oxalate in vitro produces endotoxin tolerance, i.e. a loss of responsiveness to LPS and conversely, prior exposure to LPS elicits a similar heterologous desensitization to oxalate. Renal cell desensitization to oxalate stimulation may have profound effects on the outcome of renal stone disease by impairing protective responses.

PMID: 16284883

 

I

 

So enough was enough. We consulted with several experts in the field and devised a new CR Way approach that eliminates excess oxalate and some related risk factors for oxalate accumulation. I have written about it here:

 

 

http://calorierestri...e-your-kidneys/

 

 

http://blog.livingth...organ-function/

 

 

http://www.crsociety...ended-software/

 

There is much more to say about oxalates. I am working on the oxalate issue with professionals in the kidney field and will post more about it over the next year.

 

Wishing you a healthful and not overly high in oxalate CR diet.

 

Paul

 

 

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Guest Marie

Hello,

 

Thanks for the info!

 

However, this study...

 

http://www.ncbi.nlm.nih.gov/pubmed/12187193

 

...found no correlation between high oxalate diet and oxalate in urine, or even risk of kidney stones, particularly in Caucasians. Is there a problem with the study that would lead you to question their findings?

 

Also, do you know if this particular patient was someone with underlying kidney issues, or some other condition?

 

Thanks!

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Hello,

 

Thanks for the info!

 

However, this study...

 

http://www.ncbi.nlm....pubmed/12187193

 

...found no correlation between high oxalate diet and oxalate in urine, or even risk of kidney stones, particularly in Caucasians. Is there a problem with the study that would lead you to question their findings?

 

Also, do you know if this particular patient was someone with underlying kidney issues, or some other condition?

 

Thanks!

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Ann thoughtfully provided this study and questioned the dangers of oxalate consumption in the diet. This is the study she provided:

 

Effects of 5 different diets on urinary risk factors for calcium oxalate kidney stone formation: evidence of different renal handling mechanisms in different race groups.

 

J Urol. 2002 Sep;168(3):931-6.

 

 

Rodgers AL, Lewandowski S.

 

 

Source

Department of Chemistry, University of Cape Town, South Africa.

 

 

Abstract

 

PURPOSE:

Since the incidence of renal calculi in the South African black population is extremely rare while in white subjects it occurs at the same rate as elsewhere in the western world, we investigated the possibility that different renal handling mechanisms in response to different dietary challenges might occur in the 2 race groups.

 

 

MATERIALS AND METHODS:

We administered 5 different dietary protocols, including low calcium, high oxalate, vitamin C, high salt and lacto-vegetarian, to 10 healthy male subjects from each race group. We collected 24-hour urine at baseline and after 4 days on the prescribed diet which were analyzed for biochemical and physicochemical risk factors. Dietary intake was controlled throughout the experimental period. A 24-hour dietary recall questionnaire was recorded at baseline and analyzed using food composition tables. Statistical analysis of variance was performed on all the data.

 

 

RESULTS:

The low calcium diet caused statistically significant changes only in black subjects, which consisted of urinary oxalate increase (0.17 to 0.23 mmol./24 hours, p = 0.01), relative supersaturation of calcium oxalate decrease (1.88 to 0.97, p = 0.03) and relative supersaturation of brushite increase (0.85 to 1.69, p = 0.03). The high oxalate diet caused statistically significant changes in both race groups but these changes were different in the 2 groups. In white subjects urinary pH increased (6.24 to 6.62, p = 0.01), potassium excretion increased (40.01 to 73.49, p = 0.01) and relative supersaturation of brushite increased (1.34 to 2.12, p = 0.05). In black subjects urinary citrate increased (1.94 to 2.99 mmol./24 hours, p = 0.01). Clinically unimportant changes occurred in both race groups after the other 3 diets.

 

 

CONCLUSIONS:

Renal handling of dietary calcium and oxalate in South African black and white subjects is different and may explain the different stone incidence in the 2 race groups

 

 

 

Thank you for posting this interesting study, Ann. It compares different responses of blacks and whites to a high oxalate diet. The conclusion is that the high oxalate diet produced statistically significant changes in both groups.

 

 

Do you have access to the full paper? I would like to see what the researchers considered to be a high oxalate diet. It is too bad they used 24-hour dietary recall for their study. This method is fraught with inaccuracy. Even if they had used more accurate methods of weighing dietary intake and entering into software at the time of eating, oxalate intake would still be a guessing game. AFAIK, at the time the study was published, no accurate oxalate database was available. Further the study was conducted over four days. It may take months or years for stones to form in the kidneys.

 

 

Ann asked:

 

Also, do you know if this particular patient was someone with underlying kidney issues, or some other condition?

 

It was a dietary condition: He is not unlike scores of patients my doctors see, who begin to follow diets that are high in oxalates and then develop stones.

 

We certainly don’t know all the reasons why some people develop oxalate deposits and others don’t. Many factors may singly or in combination contribute to oxalate deposits in tissues. I am glad I now have an accurate means of measuring what some of those dietary risk factors are.

 

 

Paul

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There is an excellent article about oxalic acid in the diet along with a spreadsheet of oxalic acid content in vegetables in the CR Society Insider Newsletter for the second quarter 2005. Hint: be sure you have sufficient calcium and magnesium in your diet.

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In response to my encouragement of caution when consuming high oxalate foods, Ann, one of the Society's facebook members, asked "What do Oxalates do?"

 

I wish someone somewhere could definitively answer that question. Some who follow low oxalate diets would say that oxalates are a “junk” molecule, contained in many foods: plants, nut, beans, tea, chocolate, etc. – very deleterious to health. In fact, one group I belong to advocates a very low oxalate diet, but which is full of questionable high GI, high fat, and high protein foods – not a solution for CR folk.

Happily, many aspects of a healthy lifestyle quite compatible with CR are protective against oxalate kidney stones, and therefore presumably against any other harmful effects of (calcium) oxalate, whether from the diet or not:

 

Strategies for preventing calcium oxalate stones

 

Fluid intake

The cornerstone of management is to increase urine volume. The effect appears to be linear, with a point of diminishing return reached at urine volumes of more than 2.5 L per day. We prescribe an intake of 2.5–3 L of fluids per day. [Note that CR folk often have quite large urinary volume, in part because we tend to drink fluids (green tea for health, and some to avoid hunger) but also because our high-fruit-and-vegetable, typically low-grain diets are loaded with water. Water in food counts: it's total fluid passage through the kidneys that prevents oxalate crystallization, not just the stuff that comes in a bottle or cup -MR].

 

There are data to suggest that the type of fluid ingested matters. Epidemiologic studies show that drinking coffee and beer decreases the risk of stones. Drinking grapefruit juice consistently increases stone risk for unclear reasons ...

 

Calcium

Studies of dietary calcium's effect on stone recurrence rates have led to major changes in nonpharmacologic manipulation. Epidemiologic evidence shows an inverse relation between dietary calcium intake and recurrence rates. This is probably best explained by calcium's inhibition of intestinal oxalate absorption. A randomized controlled trial (RCT) assigned men with hypercalciuria to follow either a diet low in calcium (400 mg) and oxalate or a diet higher in calcium (1200 mg) with restricted intake of oxalate, protein and salt. At 5 years, the latter group had a 51% lower rate of stone recurrence ... Although controversy persists and replication of these findings under other clinical circumstances would be desirable ...

 

Sodium

Calcium excretion is directly linked to sodium excretion. Reductions in dietary sodium reduce calciuria, but no RCT of sodium restriction alone has been performed. [This was in 2006; subsequently a successful trial was performed -- see below -MR]. The successful diet mentioned earlier that was higher in calcium and restricted intake of oxalate, protein and salt achieved a reduction in calcium excretion despite the higher calcium intake. This effect was attributed to the reduction in dietary sodium intake to less than 2 g/d.

 

Protein

The ingestion of animal protein has adverse affects on urine chemistries: it lowers citrate excretion and increases calcium and uric acid excretion. Epidemiologic data show that it correlates well with the prevalence of stone formation. ... Patients with recurrent stones should minimize their protein intake to less than 80 g/d.

 

Role of diabetes and obesity in stone formation

Recent data have suggested an increased prevalence of stones among people with diabetes and among obese people. Insulin resistance may reduce urinary citrate excretion and increase calcium excretion, and a greater body mass index is associated with increases in urinary oxalate excretion. Low urine pH is associated with increased risk of uric acid stones as well. Weight loss ... and improved diabetes control may help to prevent stone formation in appropriate patients, although this approach has yet to be tested in an RCT.

Here is the trial of a low-sodium diet that I mentioned above:

 

Am J Clin Nutr. 2010 Mar;91(3):565-70. doi: 10.3945/ajcn.2009.28614. Epub 2009 Dec 30.

Effects of a low-salt diet on idiopathic hypercalciuria in calcium-oxalate stone formers: a 3-mo randomized controlled trial.

Nouvenne A, Meschi T, Prati B, Guerra A, Allegri F, Vezzoli G, Soldati L, Gambaro G, Maggiore U, Borghi L.

 

... A total of 210 patients were randomly assigned to receive a control diet [water therapy alone: 2 L/d in the cold season (October–March) and 3 L/d in the warm season (April–September)] (n = 102) or a low-sodium diet [water therapy and a low-salt diet: "eliminate the intake of kitchen salt (including salt added to foods and salt used for cooking) and to strictly limit their consumption of food with a high salt content, as specified on the instruction sheet given to them after detailed explanations ... by a member of our team who specialized in food science] (n = 108); 13 patients (2 on the control diet, 11 on the low-sodium diet) withdrew from the trial.

 

At the follow-up visit [3 months later], patients on the low-sodium diet had lower urinary sodium (mean +/- SD: 68 +/- 43 mmol/d at 3 mo compared with 228 +/- 57 mmol/d at baseline; P < 0.001). ["On the basis of these urinary data, the spontaneous mean baseline intake of sodium chloride in [low-sodium] patients was ≈13 g/d, and it had reduced to ≈4 g/d at the follow-up visit."] Concomitant with this change, they showed lower urinary calcium (271 +/- 86 mg/d at 3 mo compared with 361 +/- 129 mg/d on the control diet, P < 0.001) and lower oxalate excretion (28 +/- 8 mg/d at 3 mo compared with 32 +/- 10 mg/d on the control diet, P = 0.001). Urinary calcium was within the normal range in 61.9% of the patients on the low-salt diet and in 34.0% of those on the control diet (difference: +27.9%; 95% CI: +14.4%, +41.3%; P < 0.001).

 

CONCLUSION: A low-salt diet can reduce calcium excretion in hypercalciuric stone formers.

 

PMID: 20042524

There is also some evidence that phytic acid (IP6) inhibits calcium oxalate stones and possibly tissue calcification. Many CR people eat a lot of IP6-rich foods, such as legumes (depending on the type and the study, 0.2-2.9% phytate by dry weight), rice bran (2.56–8.7% phytate by weight), wheat bran (2.1–7.3%), and many nuts (especially almonds, but also walnuts and pecans); indeed, the MegaMuffin might be considered a giant phyt-fest. I note that in PMID: 6094846, phytic acid was given as 10 g of rice bran, twice daily; one 240 Cal MegaMuffin contains 17 g of rice bran, plus substantial wheat bran and almonds. The highest intake in the Nurses Health Study (PMID 15111375) was >939 mg of phytate, and htis was found to be protective; PMID: 15579526 found no effect, but even the full text doesn't tell you what the range of phytic acid intake was, so this may just be a dose effect.

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Thank you, Michael! I appreciate your response on multiple levels. Any good discussion on oxalates needs to include "basics" of oxalate management and you have provided some excellent information that everyone should keep in mind. I also appreciate your response here, in this forum. As you know, I believe that posts here have communication advantages, not the least of which is that the subject stays visible, so people can respond to it when time permits. It also allows us to add to the posts over time, as new information becomes available.

 

Some CR folk consume almost 2000 milligrams of oxalate on certain days, enough if done consistently, to be of serious concern. When I was at that level, I noticed oxalate accumulation in my kidneys, which would have been a disaster if I had not monitored my kidney health with my superb physicians Drs. Rosen and Bromberg who caught it and pointed me in the direction I needed to correct the problem.

 

Many people will not be so lucky. Especially at risk are those who have a lot of internal oxalate production because of pathogenic bacteria and/or an inability to degrade oxalate because of impaired gut microflora.

 

I hope to post more about this and not leave this response without references, but the latest and exciting developments in CR research are calling, so I must go for now.

 

Paul

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Guest Tristan

Thank you for the article. Do fruit flies have coaalrpbme metabolic systems to humans. That is does Vitamin C, glycine raise oxalate levels in fruit flies. Is there any indication that their dietary products were manipulated or modified to create high oxalate levels which would not be there naturally, for example was the apple soaked or made to have an increase of oxalates? I have other questions. I am curious because I do not have access to the model which is linked to from this article.

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I'm going to resuscitate this thread. Are you guys monitoring your oxalates? It just occurred to me after I read Al Pater's citations on the asiatic star-fruit, an oxalate rich fruit, which caused kidney impairment. I often eat lots of spinach and swiss chards, last day I eat one kg, which should contain about 10 grams of oxalates, less considering it was cooked (but I drink the water). I'd just hate to give up such incredibly micronutrient-rich vegetables but of course if danger is real I'll be compelled to decrease the amount substantially. Jack Norris in his website cites a surely safe threshold of 300 mg per day, which is nothing, equalling 33 grams of spinach. He also cites Calcium and citrate as 'antidotes'. Maybe some urine analysis would help to quantify the issue, but would an high oxalate content in urine suggest an unbalanced dangerous situation ? I drink lots of water, take Ca supplements and natural phytates, although I ingest many foods rich in oxalates, not only vegetables.

Edited by mccoy

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I personally don't worry about oxalates, because while I consume quite a bit of oxalates,  I believe many of those high-oxalate foods come with in-built neutralizers - example, I consume quite a bit in the way of daily almonds and drink a lot of green tea, so high oxalate, but also protective phytates and tons of fluid. Meanwhile I also drink daily coffee and generally eat quite a bit of fluid-rich fruit. In any case, I suppose it takes time for kidney problems to occur. I've been on this type diet (more or less) for over 15 years (coming upon 20), and so far have had no problems with kidneys that I know of, and my yearly blood panel has no biomarkers which would indicate any type of kidney issues. You'd think, that if problems were building up slowly over 15-20 years, you'd see that reflected in deteriorating biomarkers (creatinine, BUN, GFR etc.), but those have been rock solid at optimal levels all this time, so what reason would I have for suspecting kidney problems? I experience no kidney pain, my urine when tested has had no alarms raised, etc. Why would I have zero problems if I have been "abusing" myself with a high oxalate diet for so long? My suspicion - it's not a problem for my particular physiology + diet combo. YMMV.

 

How prevalent are these problems with a high oxalate? I can't find good stats, so for now, the issue of oxalates does not make the list of my health concerns. Bottom line: I don't worry about this issue at all. So that's one person's account.

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The study Michael Rae points to higher up in this thread also suggests phytic acid (IP6) high in a CRON diet to be protective at least up until that now slightly dated reference. High ca++, etc. also helpful ( see full review). It would be interesting to see if Paul's position ( taking a relatively guarded position) has evolved since that time. Anybody here part of CRWay, which is Paul's private for-pay CR interest group and may have insight into his position?

 

I'd expect if Michael's feeling about it has evolved ( taking the position of risks attenuated via CR nutrition) he probably would have updated the thread but he may want to chime in to confirm.

Edited by Mechanism

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I know calcium oxalate is a risk for me. I have an unobstructing kidney stone and in the past have had oxalates in urine tests and urethra pain and bleeding from the sharp edges of the crystals. Limes and lemons are high in citric acid.

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Thanks guys for your observations, which again underline the very large variability in the response of our individual systems.

 

Since so far I observed no adverse reactions to oxalates, yet wish to prevent any potential detrimental effects, I'm going to eat one pound of spinach or swiss chard instead of 2 pounds and not every day, plus in those occasions I'm going to take double Ca supplements and make sure I drink additional water.

 

The benefits of those vegetables (to speak not of their taste!) are too many to simply cease eating them without exhibiting symptoms.

Edited by mccoy

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