My response to Owen's post regarding SCD

[Guest guest]

Some of you might remember that about two weeks ago there was a discussion

on the Low Oxalate diet here that a listmember cross-posted to the Low

Oxalate Diet list. Owens posted a heated response with a lot of words

that didn't address the issues that were raised. I was asked to comment on

's post, so here is my response. Sorry it took me so long to get this

done.

First, I stand by what I said about Vitamin D: It is a fat soluble vitamin

and must be taken with food in order to be absorbed. Taking it in between

meals means it won't get absorbed and a deficiency will develop. This might

not be a problem in the summer when the kids get sun exposure but now we are

into late fall and only people living in the lowest third of the continental

US are able to get the kind of sunshine with which they can make Vitamin D.

I suspect that many if not most of kids with chronic diseases are already

deficient in VitD; the practice of consuming it on an empty stomach will

make a deficiency worse. Saying it's " standard practice " on the low oxalate

diet to take VitD between meals avoids answering the question of whether

that advice leads to a deficiency (the answer is yes). That fact that it

was done for adults doesn't mean it's safe for children, especially sick

children.

Second, I would expect to see some improvement in some kids as some of their

oxalate burden is reduced. The problem, as I said in my paper, is that the

calcium has not been addressed and oxalate deposits are, in the end, a sign

of problems with calcium management. The fat-soluble vitamins A D & K are

what the body uses to manage calcium, all of which are not only ignored but

in fact depleted on the Low Oxalate Diet. There are plenty of kids on the

Low Oxalate Diet who are not doing so well, and I believe the reason is tied

to deficiencies in their fat-soluble vitamins which lead to calcium-handling

problems. The regressions are due, I believe, to imbalances in ionic

calcium which is bombarding the calcium channels in the neurons.

Third, in all honesty, no one has any idea whether the regressions shown by

kids on the Low Oxalate Diet are related to so-called " oxalate dumping " or

something else because none of these kids have had lab tests. Owens

is certainly not advising anyone starting on LOD to have fat-soluble vitamin

levels tested first yet that should be a requirement, since LOD will result

in depletion of D and K.

Fourth, yes Vitamin K2 is manufactured by gut flora but Vitamin K1, found in

foods like green leafy vegetables and egg yolks, is converted to K2 in the

body. K2 is found in abundance in the brain and the kidneys. Vitamin K is

recycled by the body but if recycled and dietary Vitamin K cannot be

converted into the usable form (because the enzyme, which is

sulfur-dependent, is bound to heavy metals) or if there are perhaps genetic

problems slowing the " activation " portion of the K cycle, then a " leak " will

develop pretty quickly and a Vitamin K deficiency ensues. I believe that

all the kids, and probably other family members too by the way, have

deficiencies in this vitamin and would benefit from taking K2. Moreover,

these is no pattern at this time in whether kids on SCD or LOD or any other

diet show more or less response to Vitamin K2 because not many parents have

tried this supplement yet, especially in high doses. But I believe that the

kids' improvement on K2 has nothing to do with whether they were on a

high-oxalate or low-oxalate diet - they seem to be universally deficient.

BTW Vitamin K is also a fat-soluble vitamin that must be consumed with food.

Fifth, I completely agree with her that oxalates are a big problem in not

only autism but many other chronic diseases also.

And finally, I kind of like her admission at the end:

>That doesn't mean EVERYTHING

>about that diet [Low Oxalate Diet] is healthy. Time will tell!

SCD has certainly stood the test of time - there is nothing unhealthy about

it. If there are unhealthy aspects to LOD, why put your sick child on it?

Why not just supplement the fat soluble vitamins instead?

PS If anyone wants to cross-post this please ASK my permission first.

>

>

>Lorilyn,

>

>I want to correct some things that said.

>

>

> >The Low Oxalate Diet was originally designed

> >as a stopgap measure, to bring pain relief to adults with vulvar

> >pain while they used other measures to try to reduce their oxalate

> >load. It was not designed for children, was not intended to be used

> >long term, and will result in chronic nutritional deficiencies.

>

>The Low Oxalate Diet was not developed by Clive Solomons or the VP

>Foundation with which he works. He became interested in using this

>therapy

>at least several decades after it had been used extensively by

>people with

>certain types of kidney disease, and that would include children.

>People

>with kidney disease stay on the diet for life, and I have seen

>nothing in

>the literature concerned about it inducing nutritional or vitamin

>deficiencies, although vitamin deficiencies can lead to oxalate

>problems.

>

> From http://www.emedicine.com/med/topic3027.htm

>

>Please note the advice to exclude vitamin D from the calcium taken

>at

>mealtime to bind oxalate. This was not my invention. It is

>standard practice.

>

>===================

>Enteric hyperoxaluria: Several mechanisms have been postulated to

>help

>explain the development of hyperoxaluria in patients with intestinal

>disease. These include increased colonic permeability, reduced free

>intestinal calcium available to complex with oxalate, and a decrease

>in the

>quantity of Oxalobacter formigenes in the intestine (which can

>degrade

>intestinal oxalate). In any event, the intestinal absorption of

>oxalate is

>markedly increased. Based on the pathophysiology, pyridoxine has

>only a

>limited beneficial effect in this condition because endogenous

>oxalate

>production is not affected.

>

>... o The most commonly recommended form [of calcium] is

>calcium

>citrate because the citrate component offers an additional benefit

>as a

>natural inhibitor of calcium oxalate urinary crystallization.

>Calcium

>citrate without vitamin D should be used because the calcium should

>remain

>in the intestinal tract as long as possible to better interact and

>bind

>with the available oxalate. Calcium carbonate can also be used, but

>it does

>not have the same beneficial effect as citrate.

>

>=========================

>

>I've told this to privately, but she still doesn't get

>it: Dr.

>Solomons is not an oxalate researcher, and that is obvious since it

>never

>ocurred to him to investigate bowel concerns in these women. He is

>a

>specialist in connective tissue disorders. He PRESUMED there was an

>endogenous production of oxalate but this was just his GUESS because

>he did

>not know the oxalate literature showing that the body stores

>oxalates and

>releases them for YEARS after the source of the oxalates has been

>removed. Dr. Solomons was treating a condition where the only thing

>they

>were trying to change and their measurement of success was whether

>or not

>the women had any more vulvar pain.

>

>This is a different issue from restoring neurological function and

>it is

>much easier to tell when your goal is reached. With the children on

>the

>low oxalate diet for autism, we keep being pleasantly surprised

>about

>positive gastrointestinal and neurological changes still occurring

>in these

>children as long as a year into the diet. We do not know the

>potential of

>the diet if it is done for longer than sixteen months, although we

>are

>getting reports that some of the children who have been on the diet

>the

>longest are still having " dumping " symptoms and improvements. These

>episodes should stop when the process of eliminating body stores is

>complete and when the levels of oxalate in urine or other secretory

>site

>stay low all the time. as described in the kidney literature.

>

>Just so you'll know, the literature on the release of stored oxalate

>comes

>from measurements of plasma oxalate in liver transplant patients who

>lost

>the source of their excess oxalate when they lost their defective

>liver. This process of the oxalate levels skyrocketing during the

>first

>releases of oxalates from tissues, followed by the slow ratchetting

>down of

>oxalate levels has been shown to continue as long as four years, but

>over

>that period it is known that organs damaged by oxalate are gradually

>restored to normal function. We don't know where oxalates have

>caused

>damage in autism, but the nature of the improvements we see on this

>diet

>over the term of a year are certainly giving us hints!

>

>I've also already mentioned to that I attended the world

>oxalate

>conference run by FASEB two summers ago and learned that Dr.

>Solomons's

>work is not upheld in the oxalate field because of the way he

>wouldn't

>discuss his techniques of measurement and due to his lack of peer

>review. After several conversations with his wife, I also became

>as

>concerned as the kidney people about the silence regarding the way

>he did

>his measurement of oxalate...but that is not to negate the benefit

>the

>women are getting on the low oxalate diet coupled with using some of

>his

>methods of repairing connective tissue that was damaged by oxalate.

>I am

>really happy that he made clear the association of oxalate with

>pain, as

>this was really what got us looking at oxalates in the first

>place...to see

>if lessening the exposure to oxalate would decrease pain in the gut

>in

>children with autism. We did not expect to see such obvious " dumps "

>with

>such quick cycles in neurological function and intestinal health

>that

>listmates have reported. These changes outside what is described in

>the

>literature and happening with the diet are what obligated us to do

>the work

>to get this studied properly with appropriate funding and controlled

>studies.

>

>Endogenous excess production of oxalate may come from B6 deficiency

>which

>replicates the error in primary hyperoxaluria type 1. This may have

>relevance to the benefits described in autistic patients in studies

>that

>Rimland reported at:

>http://www.autismwebsite.com/ARI/treatment/b6studies.htm.

>

>I do encourage listmates to make sure they are taking the vitamin

>cofactors

>whose lack can lead to some endogenous production, but the vitamins

>will do

>absolutely no good if the problem instead is enteric

>hyperabsorption. There is no science at this point to support

>Solomons

>thinking that the body steps up oxalate production on a low oxalate

>diet.

>That was total conjecture on his part born out of lack of

>familiarity with

>the scientific literature which had a more obvious explanation.

>

>Plants have special cells in which they step up production of

>oxalate to

>deal with the toxicity of calcium or other metals, but there is no

>research

>showing this process being at work in mammals, or an equivalent type

>of

>cell. Oxalate is not nutrititive. It is considered an

>antinutrient. Plants make ascorbic acid to convert to oxalate to

>limit the

>toxicity of the calcium in the plant, sequestering the calcium

>oxalate

>formed from this interaction in special cells called idioblasts.

>Without

>this process, the excess level of calcium in the plant would injure

>or kill

>the plant. Right now, there is not any research showing a positive

>side to

>oxalates in humans, so why would the body make more when it is

>basically

>considered to be the trash?

>

>Enteric hyperabsoption of oxalate doesn't always, but it can raise

>oxalate

>levels as high as the genetic defects and it is far more important

>and its

>levels are so much more relevant than the endogenous production

>

>hinted at. For instance:

>

>Barbey F, Cachat F, Nguyen QV, Rotman S, Burnier M, Daudon M.

>[Massive

>hyperoxaluria] Rev Med Suisse Romande. 2004 Aug;124(8):477-82.

>

> Primary hyperoxaluria type I is a rare inborn error of

>metabolism

>caused by a deficiency of a liver-specific peroxisomal enzyme. It

>manifests

>by increased oxalate production that ultimately results in kidney

>failure,

>due to urolithiasis and nephrocalcinosis, and finally induces

>systemic

>oxalosis and risk of premature death. Primary hyperoxaluria type 2

>is

>mainly responsible of urolithiasis. Enteric hyperoxaluria is a

>commonly

>seen adverse event of Crohn disease or after extensive intestinal

>resection. These affections represent the main etiologies of massive

>hyperoxaluria. If not recognized very soon and adequately treated,

>these

>conditions can progress rapidly to end stage renal failure. PMID:

>15495471

>

>The oxalate field has not quite caught up with the idea that

>sometimes this

>massive absorption is taking place without damaging the kidneys, so

>showing

>that this can occur will be an important part of our project's

>scientific

>goals. Only rarely does a child with autism have kidney stones or

>other

>serious urinary problems, but in an uncontrolled study, Bill Shaw's

>lab

>found that 36% of the children he measured on the autism spectrum

>had

>oxalate in urine that was higher than 90 mmol/mol creatinine, which

>is the

>cutoff for primary hyperoxaluria. This doesn't mean they have

>primary

>hyperoxaluria (for it is hereditary) but it does suggest that their

>excess

>oxalate absorption may be quite severe.

>

>One study we are planning to do might help the SCD community to

>understand

>whether they are adequately preventing oxalate absorption in the

>gut. This

>would involve measuring blinded samples from SCD, g/f c/f, and

>untreated

>autistic children to see how these groups compare in urinary oxalate

>levels.

>

>Samples from the low oxalate dieters would be difficult to compare

>to these

>groups since it is known that oxalate release from tissues can be

>much

>higher than levels ever were before the elimination of the reason

>for

>excess absorption. Some of our LOD subjects might be experiencing a

> " dump " , and then others would not, and it would be very fuzzy data

>to

>combine them. For that reason, to address this issue, we will be

>doing

>blinded studies following people on this diet during these " dumping "

>periods so that we can better understand this phenomenon that is not

>well-described in the literature. We will correlate clinical

>observations

>of these children with the results of the lab tests. Unfortunately,

>this

>study will have to wait until we can perfect the techniques

>necessary to

>measure oxalate in stool, plasma, and sputum. When these tests are

>available, then we will be able to test the effects of other

>treatments

>like yogurt, different probiotics, LDN and HBOT on oxalate

>elimination, and

>can also monitor changes in oxalates that might occur during anti-

>fungal or

>antibiotic treatment.

>

>There is an enormous liiterature on enteric hyperabsoprtion which is

>related to kidney disease. However, kidney doctors and scientists

>did not

>consider that the oxalate in the diet may keep the intestinal

>tissues

>irritated if they are already injured. That effect would keep the

>tissues

>from healing properly. We are certainly suspecting this process of

>continued injury might have been occurring in those whose intestines

>did

>not heal on a high oxalate diet but did on a low oxalate diet.

>

>The proof that the gut must be working better at getting nutrition

>to the

>rest of the body is testified to by the frequency of reports of

>children

>who did not grow on SCD but have had amazing catch-up growth on

>LOD. Measuring growth is a very objective measure, and I encourage

>the

>pecanbread listmates to watch growth carefully.

>

>As Lorilyn pointed out, the early SCD diet is basically a low

>oxalate

>diet. If pecanbread listmates follow the advice to not step up the

>introduction of the higher oxalate foods until the gut is healed,

>then the

>lack of oxalate in early SCD may be a larrge part of what heals the

>gut. Why suspect that mechanism versus something involving

>disaccharides? Oxalates bind DAMAGED tissue, and ignore undamaged

>tissue,

>but once they bind damaged tissue, they get taken into cells and

>turn on

>inflamatory factors and deplete glutathione. Once the inflammation

>in the

>gut is over, then the oxalate in the diet should not further damage

>the gut

>when the later high oxalate foods are introduced.

>

>I say that with a BIG warning, however, because even after the gut

>is

>healed, there may still be reasons for an excess absorption of

>oxalate

>through open tight junctions between cells. I'm talking about what

>happens

>after the upper intestinal tissues themselves are healed and the

>pain is

>gone. For instance, a study I've put below shows that by eating a

>high

>oxalate diet, that the percent of oxalate absorbed from that diet

>will

>double in someone perfectly normal...with no gut inflammation. In

>this

>study in the persons on low oxalate diet, presumably the oxalate

>absorption

>would have been about 5 mg, but on the 600 mg oxalate diet, the

>absorption

>would have been 88 mg. which is almost twenty times as much. Does it

>make

>sense, then, to eat a high oxalate diet on SCD even after the gut is

>healed?

>

>What we seem to be seeing on the LOD is that oxalates have caused

>neurological damage (whether direct or indirect) and may have caused

>other

>issues in the body like stiffness and an inability to initiate or

>sustain

>and plan movement. We notice that up to this point neurological

>improvements continue the longer listmates have been on the diet .

>In

>fact, one prize of sticking with the diet for many months appears to

>be big

>increases in executive function. Now, considering that, if someone

>inappropriately followed Dr. Solomon's advice to use the alleviation

>of

>pain as the indicator of when to start introducing higher foods,

>then these

>children would never have gotten to the cognitive improvements. The

>good

>news is that we are even starting to see those sorts of improvements

>in

>adults with autism!

>

>Now on another matter, our flora, not our food, provides vitamin K2,

>and

>that comprises 80-95% of the liver vitamin K supply. Also, each

>molecule

>of vitamin K is recycled several thousand times before it is

>degraded.

>(Vermeer, 1990) That means that anything that might impair that

>recycling

>process would have far more effect on vitamin K sufficiency than any

>difference in diet or in floral manufacture of the vitamin. What

>recycles

>vitamin K? Thiols. These are the very molecules that may be

>impaired in a

>high oxalate environment because high oxalate levels oxidize thiols,

>rendering them useless for use by reductases.

>

>We don't have data to compare whether SCD or LOD does a better job

>of

>ensuring the flora is making adequate vitamin K, but what is the

>evidence? Vitamin K deficiency is reported in inflammatory bowel

>conditions which are the very conditions that experience excess

>absorption

>of oxalate. There are no reports of vitamin K deficiency developing

>in

>those on the low oxalate diet despite its use for decades. Is the

>community of microbes in the gut more capable of making vitamin K2

>when

>oxalates in the diet are reduced? One thing that may give us

>insight in

>this area is whether those reporting big benefits from taking

>vitamin K2

>are people who are staying with a high oxalate version of SCD, or

>those who

>are doing a low oxalate diet. I also find it interesting that a

>quarter of

>the listmates who made the switch to LOD and answered a survey

>reported

>losing dysbiosis when under previous diet they were having to be

>constantly

>under antifungal medication. So, was the proper gut flora happier

>with a

>high or with a low oxalate environment? What about the " bad flora " ?

>

>So, if SCD had so much better a supply of vitamin K to the body than

>the

>low oxalate diet, why are the big responders to the vitamin K

>therapy

>coming from those who were a long time on SCD and are preferring to

>go back

>to it? Were they offered dehydrators, ice cream machines or bananas

>to get

>them back into the SCD camp? (What craziness is that!) Can

> tell

>us the ratio of responders to non-responders to vitamin K therapy

>compared

>to their diet status?

>

>That will have to do for tonight. The pecanbread moderators have

>put so

>many requirements on their ex-SCDers that I doubt too many qualify,

>especially because I advise changing probiotics to the oxalate-

>degrading

>VSL#3. Perhaps some ex-SCDers did not shift probiotics because of

>the fear

>of the casein or corn starch in the product.

>

>Anyway, I appreciate the boldness of those who have been willing to

>answer

>the request of the pecanbread staff, but I don't want our listmates

>to feel

>obligated to be open themselves up for criticism of how they did SCD

>when

>they are no longer adherents of that diet, anyway, but if you want

>to

>answer them, that's OK. This diet will not stand or fall because of

>criticism of those with another diet. The proof is in the pudding.

>If LOD

>works, then no one is going to stop it gaining adherents just like

>no one

>stopped SCD when it first was introduced because it could deliver on

>the

>ability to quell intestinal inflammation in many people. That

>doesn't mean

>EVERYTHING about that diet is healthy. Time will tell!

>

>By the way, SCDers, please learn how to spell oxalate!

>

>

>