Owens? Elevated B12, tics, etc

[Guest guest]

Hi --

I am confused with what you are saying here. Are tics related to oxalates or

are you saying that you could look at a situation like Miralax to draw

analogies? Are the quantities of xylitol in daily chewing gum enough to

cause

basal ganglia problems?

Thanks,

In a message dated 8/20/2005 6:27:57 AM Pacific Standard Time,

csb-autism-rx writes:

Message: 4

Date: Fri, 19 Aug 2005 22:52:42 -0500

Subject: Re: Elevated B12 in blood test, tics, liver accumulation etc

Jaquelyn and ,

I think there are some hints at what is happening to be garnered from

observations about adverse effects from Miralax or Glycolax. There is

pretty good circumstantial evidence that the problem when there are adverse

reactions to this constipation medication may be from the PEG becoming

metabolized by gut flora and then further converted into oxalates. There

are a few children on the Miralax list that developed clear cases of

calcium oxalate issues in the kidneys associated with PEG use. Some

parents have reported the onset of tics with miralax and their resolution

when discontinuing Miralax. Again, the issue may be that the Miralax was

producing oxalates.

Do oxalates get to the basal ganglia? Yes. Might this be related to how

certain SSRI's work? Yes. Experimentally, do scientists physically link

serotonin to oxalate? Yes. Are there associations of hyperoxaluria with

basal ganglia disease? Yes.

The last article in the first section of abstracts should be seen in the

context of knowing that the sugar substitute xylitol has the distinctive

record of producing serious and even fatal basal ganglia and renal disease

associated with oxalates if given in high enough quantity....but what does

it do at a lower quantity?

A little over a year ago I started a list (very inactive now) for people

who saw elevations of hippuric acid along with their development of PANDAS

after a strep infection. Hippuric acid is a regulator of the glutathione

chemistry especially in the kidneys, but it is also a regulator of a

molecule called an oxalyl thiolester that nobody knows about. Hippuric

acid makes oxalate crystals dissolve, but why would it be stepped up after

a strep infection, and what happens to the oxalate after that? There is a

lot to sort out.

1: Neuroradiology. 2005 Feb;47(2):105-7. Epub 2005 Feb 16.

Bipallidal haemorrhage after ethylene glycol intoxication.

Caparros-Lefebvre D, Policard J, Sengler C, Benabdallah E, Colombani S,

Rigal M.

Service de Neurologie, CHU Pointe a Pitre, Guadeloupe 623, Av de la

Republique,

59800 Lille, France. dcaparros@...

Acute or subacute bipallidal lesion, an uncommon radiological feature produced

by metabolic disorders or poisoning, has never been attributed to ethylene

glycol (EG) intoxication. This 50-year-old Afro-Caribbean alcoholic man had

unexplained loss of consciousness. Blood tests showed osmolar gap. Drug

screening was positive for EG at 6.06 mmol/l. Brain CT revealed bilateral

pallidal haemorrhage. Pallidal haematoma, which could be related to deposition

of oxalate crystals issued from EG metabolism, should lead to toxicological

screening.

Publication Types:

Case Reports

PMID: 15714272 [PubMed - indexed for MEDLINE]

2: J Neurophysiol. 1999 Jul;82(1):69-85.

Serotonergic modulation of neurotransmission in the rat basolateral amygdala.

Rainnie DG.

Harvard Medical School and Brockton Veterans Affairs Medical Center,

Department

of Psychiatry, Neuroscience Laboratory 151C, Brockton, Massachusetts 02301,

USA.

..... In interneurons 5-hydroxytryptamine oxalate

(5-HT) evoked a direct, dose-dependent, membrane depolarization mediated by

a 45

+/- 6.9 pA inward current, which had a reversal potential of -90 mV. The

effect

of 5-HT was mimicked by the 5-HT2 receptor agonist,

alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT), but not by the 5-HT1A

receptor agonist, (+/-) 8-hydroxydipropylaminotetralin hydrobromide

(8-OH-DPAT),

or the 5-HT1B agonist, CGS 12066A....

PMID: 10400936 [PubMed - indexed for MEDLINE]

3: Neuroradiology. 1984;26(6):517-21.

Reno-cerebral oxalosis induced by xylitol.

Ludwig B, Schindler E, Bohl J, Pfeiffer J, Kremer G.

A 20-year-old man suffering from Crohn's disease developed coma and

generalized

seizures following ileocecal resection. During postoperative parenteral

feeding

he received xylitol in an unusually high concentration. CT examinations a few

days before death showed intense hypodensity and swelling of brainstem and

basal

ganglia and increasing triventricular dilatation. Autopsy revealed, mainly in

the brainstem and cerebellum, a destruction of intracerebral, intracerebellar

and leptomeningeal vessel walls by birefringent crystals (probably calcium

oxalate), an early inflammatory reaction and severe brain edema with final

tonsillar herniation. The same crystalloid deposits were found in the kidneys.

Publication Types:

Case Reports

PMID: 6438546 [PubMed - indexed for MEDLINE]

==================

Hippuric acid and oxalates

1: Clin Chem Lab Med. 2001 Mar;39(3):218-22.

Hippuric acid as a modifier of calcium oxalate crystallisation.

Laube N, Jansen B, Schneider A, Steffes HJ, Hesse A.

Department of Urology, Bonn University, Germany. laube@...

Hippuric acid (HA) originating from the conjugation of benzoic acid with

glycine

is a physiological component of human urine. Findings suggest that HA inhibits

calcium oxalate (CaOx) growth and considerably enhances the CaOx solubility in

artificial urine. Thus, it is assumed that HA is a major modifier of CaOx

formation. However, only a slight CaOx growth inhibition of 1-8% was also

reported. These values were also derived from artificial urine. The key

mechanism, which led HA to be of interest in urolithiasis research is the fact

that in presence of Ca2+ ions HA can form a hippurate complex. By forming

such a

complex, Ca2+ concentration in urine decreases, and as a consequence, CaOx

formation is inhibited. This study was performed in order to clarify the

role of

HA in native and artificial urine. Biochemical analyses to calculate the

relative CaOx supersaturations and crystallisation experiments using an

in-line

laser probe were examined. BONN Risk Indices indicating the risk of CaOx

crystallisation were calculated from the results of the crystallisation

experiments. The results obtained from artificial as well as from native

urines

showed that HA has no significant effects on CaOx formation. We suggest that

HA

plays only a minor role as a crystallisation modifier in human urine.

PMID: 11350018 [PubMed - indexed for MEDLINE]

2: Urol Res. 1993 May;21(3):181-5.

Solubility, inhibited growth and dissolution kinetics of calcium oxalate

crystals in solutions, containing hippuric acid.

Gutzow I, Atanassova S, Budevsky G, Neykov K.

Institute of Physical Chemistry, Bulgarian Academy of Sciences, Sofia.

An analysis of crystal growth and dissolution of slightly soluble salts in

physiological solutions in the presence of complexing ions was carried out,

simulating conditions typical in human urine. It was found that hippuric

acid, a

normal physiological constituent of urine, acts at increased concentrations

as a

dissolving agent with respect to calcium oxalate (CaOx) and CaOx calculi. The

kinetics of dissolution of crystalline CaOx calculi in physiological solutions

containing hippuric acid at different concentrations were studied, using the

change in the Archimedean weight of samples immersed in the solution. Analysis

of the experimental results enabled the determination of the increased

solubility of CaOx in the presence of hippuric acid and the quantitative

characterization of this substance as a new and promising agent for dissolving

CaOx calculi in human urine. The possible effect of hippuric acid as a natural

regulator of CaOx supersaturation and crystallization in human and mammalian

urine is also discussed.

PMID: 8342252 [PubMed - indexed for MEDLINE]

3: Vet Hum Toxicol. 1982 Oct;24(5):331-4.

Urine and tissue oxalate and hippurate levels in ethylene glycol

intoxication in

the dog.

Riley JH, Stahr HM, O'Brien S, Riley MG.

Oxalate, hippurate and ethylene glycol were measured in dogs given 5 ml/kg

ethylene glycol orally. Eight hours after administration, oxalate levels were

7.2-9.1 ppm in renal tissue and 10-100 ppm in urine. Hippurate was 40-90 ppm

in

urine. Ethylene glycol was 10-100 ppm in renal tissue and 5,300-27,000 ppm in

urine. The above substances were measured in urine and renal tissue from

normal

dogs, dogs in non-toxic renal failure and clinical cases of ethylene glycol

intoxication. Urine was analyzed for ethylene glycol by gas chromatography

using

direct injection. Ethyl ether extraction provided good recovery of ethylene

glycol from tissues and blood. Results were confirmed by gas

chromatography/mass

spectrometry (GC/MS). Oxalic acid (CA oxalate) was extracted with acidic

methanol, methylated and analyzed by GC. Results were confirmed by GC/MS.

Hippuric acid (calcium hippurate) was extracted with acidic methanol and

chromatographed by thin layer chromatography (TLC). Ultraviolet

spectrometry and

mass spectroscopy were used to confirm the results. High performance liquid

chromatography (HPLC) and TLC with densitometry were used to quantitate

hippuric

acid.

PMID: 7135799 [PubMed - indexed for MEDLINE]

At 04:44 PM 8/19/2005 -1000, you wrote:

>: This is an impossible question for me to answer, but I have not heard

>of an irreversible tic problem with MB-12. However, there may be some risk

>in everything we do - we have to use our intuition plus medical knowledge to

>try to come up with risk/reward ratio. Having autism is risky too. So far,

>I have found injectable MB-12 to be primarily beneficial in the majority of

>children using it, and almost miraculous in a sizeable number of children,

>so will continue to prescribe it for all my patients unless I get

>new/contradictory information. However, there are no guarantees and the

>parent always has to make the final choice about any particular treatment.

>Believe me, I've tried many things in Chelsey that haven't worked, some

>pretty disastrous (SSRI's, stimulants) but fortunately reversible.

>

>I did find this on tics:

>Tics (Pediatric) Mechanism

>The cause of tics and these associated disorders is not known. The

>association with other basal ganglia disorders suggests that tics may

>represent release phenomena with insufficient inhibition by the basal

>ganglia.