Re: VERY URGENT - Andy please - 5 yr old reaction dmsa
- Subject: Re: VERY URGENT - Andy please - 5 yr old reaction dmsa
- Date: Sun, 29 Aug 2004 15:41:05 -0500
- Yahoo! Message Number: 118898
- Onibasu Link: http://onibasu.com/archives/am/118898.html
Patricia,
One well-known cause of nystagmus is low thiamine. Medline brings up 55
articles on this association which I studied at length a number of years
ago when a friend's grandchild acquired nystagmus after her first
immunizations..
Thiamine is a sulfur compound that enhances the endocytic pathway which
helps cells recycle protein and sulfur in particular.
There are several articles below which suggest that thiamine in a
derivative form participates in thiol disulfide exchange, a process which
is extremely important to the function of the kidneys in regulating body
sulfur supplies. If thiamin derivatives for a disulfide molecule, then it
is likely that this disulfide form could interact with DMSA. We probably
don't know enough to know if it is the derivative of thiamine that relates
to nystagmus or thiamine itself. Even so, if your child was just
borderline on being deficient, and this whalloping dose of DMSA went after
that scarce commodity, it might have been just enough to tweak her over the
edge back into deficiency. Speech is also a problem in severe thiamine
deficiency, creating a condition called Wernicke's
encephalopathy...something that happens with alcoholism A LOT.
Fortunately, IF thiamine is the issue here, then giving her thiamine should
resolve the problem very quickly. Another little perk is that thiamine
(probably by increasing endocytosis) helps chelation, as an article below
reports.
Thiamine is really important for the function of lysosomes. They are the
organelle of the cell where mercury collects after a few days after
exposure, and there it gets royally stuck, and it is my opinion that this
slow-down of sulfur recycling in the kidney is one of the worst
consequences of mercury toxicity.
I think there is a good chance that DMSA meets mercury in the lysosome of
cells after the molecule has been endocytosed into cells with extremely
rapid membrane turnover like macrophages (such as the liver Kupffer cells)
and kidney tubule cells. Fortunately, these are the same cells that would
have grabbed up the mercury and gotten it out of circulation pretty quickly
after exposure.
Any time you have a period of catabolism (rapid weight loss, for instance)
the demands on thiamine go way up as cells try to recycle all that the body
is breaking down, so this can be behind the onset of thiamine deficiency,
as was the case in the report below of someone who had experience weight
loss before surgery.. It is not always "diet" that causes thiamine to
become deficient.
Of course, you may have heard of Derrick Lonsdale's work with TTFD, a
thiamine-related compound. Some DAN! doctors have reported that when used
at the same time as a chelating agent, that it enhanced chelation, even
though the molecule itself is not a chelator. Makes sense, actually. I've
put two abstracts from studies that Dr. Lonsdale has written, one that is
hot off the press. (Actually, epublished early!)
Hope this helps!
Susan
PS. Patricia, if your daughter's nystagmus was congenital, there is a
chance that you were thiamine deficient during pregnancy. Were you a mom
who got nauseous and threw up a lot during pregnancy? That could do
it. If this applies, then when you get the thiamine to help your daughter,
why don't you try some, too, and see what might change for the better!
343fc748.jpg
Thiamine
Histochem J. 1996 Mar;28(3):217-25. Related Articles, Links
Histochemical localization of autometallographically detectable
mercury in tissues of the immune system from mice exposed to mercuric chloride.
Christensen MM.
Institute of Neurobiology, University of Aarhus, Denmark.
The distribution of mercury in the spleen, liver, lymph nodes, thymus
and bone marrow was studied by autometallography in mice exposed to
mercuric chloride intraperitoneally. Application of immunofluorescence
histochemistry and an autometallographic silver amplification method was
employed to the same tissue section. Mercury was not only detected in
macrophages marked by the antibody M1/70 but also in macrophage-like cells,
which were either autofluorescent or devoid of fluorescent signals. These
two cell types were identified as macrophages at the electron microscopical
level. Autometallographically stained macrophages were observed in the
spleen, lymph nodes, thymus and in Kupffer cells of the liver. Furthermore,
mercury was observed in endothelial cells. No obvious pathological
disturbances were observed at light and electron microscopical level. At
the subcellular level mercury was localized in lysosomes of macrophages and
endothelial cells.
PMID: 8735289 [PubMed - indexed for MEDLINE]
Ann Fr Anesth Reanim. 2001 Jan;20(1):40-3. Related Articles, Links
[Click here to read]
[Postoperative encephalopathies: thiamine deficiency, an unrecognized
etiology]
[Article in French]
Vidal S, Andrianjatovo JJ, Dubau B, Winnock S, Maurette P.
Departement d'anesthesie-reanimation III, CHU Pellegrin, 33076
Bordeaux, France.
We report the case of a patient who experienced a postoperative
Wernicke encephalopathy 8 days after a left hepatectomy performed for
metastasis related to a rectal cancer. During the six months before surgery
the patient lost 10 kg of weight (15%). [catabolism increases thiamine
deficiency-sco]
Moreover, in the postoperative period the patient received exclusively 5%
dextrose solution intravenously. On the 8th postoperative day, an
alteration of consciousness, a vertical nystagmus and an ataxia led to
consider the diagnosis of thiamine deficiency that was then established by
the decrease in the transcetolase activity of the red blood cells. {a test
which confirms thiamine deficiency]
Vitamin B1 [thiamine] supply improved the clinical status rapidly and
completely. [The good news!] This observation allows to review aetiologies
and clinical forms of thiamine shortage. In addition, it stresses the
detection of exposed patients and the prevention methods.
Publication Types:
* Case Reports
PMID: 11234577 [PubMed - indexed for MEDLINE]
Hum Exp Toxicol. 2000 Sep;19(9):523-8. Related Articles, Links
[Click here to read]
Effect of thiamine on the cadmium-chelating capacity of thiol compounds.
Tandon SK, Prasad S.
Industrial Toxicology Research Centre, Lucknow, India.
The influence of thiamine on the efficacy of
meso-2,3-dimercaptosuccinic acid (DMSA), diethyldimercapto succinate
(DEDMS), alpha mercapto-beta-(2-furyl) acrylic acid (MFA) and
alpha-mercapto-beta-(2-thienyl) acrylic acid (MTA) to mobilize cadmium and
reverse cadmium-induced biochemical alterations was investigated in
cadmium-exposed rats. The thiamine coadministration enhanced the efficacy
of MFA and MTA in reducing hepatic and renal burden of cadmium and that of
DMSA and DEDMS in mobilizing hepatic cadmium. It also improved the efficacy
of DMSA, DEDMS and MFA in reversing the cadmium-induced increase in urinary
alkaline phosphatase and aspartate and alanine amino transaminases. The
combined treatment with thiamine and DMSA or MFA restricted the urinary
loss of zinc and that with thiamine and DEDMS reduced the loss of fecal
copper, a general effect of chelation. In conclusion, the administration of
thiamine during chelation therapy in cadmium poisoning may be beneficial
and more effective than thiol chelating agents alone, which needs to be
confirmed in humans.
PMID: 11204555 [PubMed - indexed for MEDLINE]
Neuro Endocrinol Lett. 2002 Aug;23(4):303-8. Related Articles, Links
Treatment of autism spectrum children with thiamine tetrahydrofurfuryl
disulfide: a pilot study.
Lonsdale D, Shamberger RJ, Audhya T.
Preventive Medicine Group, 24700 Center Ridge Road, Westlake, OH
44145, USA. dlonsdale
OBJECTIVES: In a Pilot Study, the clinical and biochemical effects of
thiamine tetrahydrofurfuryl disulfide (TTFD) on autistic spectrum children
were investigated. SUBJECTS AND METHODS: Ten children were studied.
Diagnosis was confirmed through the use of form E2, a computer assessed
symptom score. For practical reasons, TTFD was administered twice daily for
two months in the form of rectal suppositories, each containing 50 mg of
TTFD. Symptomatic responses were determined through the use of the computer
assessed Autism Treatment Evaluation Checklist (ATEC) forms. The
erythrocyte transketolase (TKA) and thiamine pyrophosphate effect (TPPE),
were measured at outset and on completion of the study to document
intracellular thiamine deficiency. Urines from patients were examined at
outset, after 30 days and after 60 days of treatment and the concentrations
of SH-reactive metals, total protein, sulfate, sulfite, thiosulfate and
thiocyanate were determined. The concentrations of metals in hair were also
determined. RESULTS: At the beginning of the study thiamine deficiency was
observed in 3 out of the 10 patients. Out of 10 patients, 6 had initial
urine samples containing arsenic in greater concentration than healthy
controls. Traces of mercury were seen in urines from all of these autistic
children. Following administration of TTFD an increase in cadmium was seen
in 2 children and in lead in one child. Nickel was increased in the urine
of one patient during treatment. Sulfur metabolites in urine did not differ
from those measured in healthy children. CONCLUSIONS: Thiamine
tetrahydrofurfuryl disulfide appears to have a beneficial clinical effect
on some autistic children, since 8 of the 10 children improved clinically.
We obtained evidence of an association of this increasingly occurring
disease with presence of urinary SH-reactive metals, arsenic in particular.
Publication Types:
* Clinical Trial
PMID: 12195231 [PubMed - indexed for MEDLINE]
Med Sci Monit. 2004 Aug 20;10(9):RA199-RA203. [Epub ahead of print] Related
Articles, Links
Thiamine tetrahydrofurfuryl disulfide: a little known therapeutic agent.
Lonsdale D.
Preventive Medicine Group, Westlake, Ohio,U.S.A.
Thiamine tetrahydrofurfuryl disulfide (TTFD) is the synthetic
counterpart of allithiamine, occurring naturally in garlic. Allithiamine
was discovered in Japan in 1951. Its extensive research was reported by a
group known as the Vitamin B Research Committee of Japan, and given this
name because of its existence in the bulbs of many of the allium species of
plants. It was found to be a disulfide derivative of thiamine, produced as
a result of enzymatic action on the thiamine molecule in garlic bulbs when
the bulb is cut or crushed. Subsequent experimental work in both animals
and human subjects revealed that its metabolic effect was much more
powerful than the thiamine from which it was derived. Japanese
investigators created a number of synthetic forms and investigated their
use in a number of human disease conditions. Although some derivatives have
been synthesized without a disulfide bond in the molecule, these
investigators emphasized that the disulfide was an extremely important part
of its biologic action and TTFD is the most modern of the disulfide
derivatives. Because at least part of its beneficial effects are the same
as water soluble thiamine salts, this review deals first with the clinical
uses of thiamine (vitamin B1) in medicine.
PMID: 15328496 [PubMed - as supplied by publisher]
At 04:41 PM 8/29/2004 +0000, you wrote:
Hello Andy, sorry to bother on a sunday. My 5 year old ASD girl (30lb) was=
put by a
"specialist" on dmsa for heavy metal treatment. Her great plains mineralog=
ram (hair)
showed middle high mercury, tin, nickel, antimony.
His protocol was 50mg dmsa once a day during 3 days and 11 off. We have do=
ne 2 cycles
and my little one has lost her pain sensitivity (which she had recoved 3 ye=
ars ago through
diet) and is losing sight. She was born with a congenital nystagmus which=
means her eyes
move from side to side and has trouble focusing, but she could find us at a=
distance of
aprox 50-60 ft and now 10ft from her she cannot see us. Night vision is eve=
n worse. I´m
afraid the mercury has redeposited in her optic nerve or worse?
Language improved greatly towards the end of the first cycle but went back=
again after the
2nd dose and has not improved since. Tolerance is also going down.
We are scheduled to start a 3rd round of dmsa tomorrow, but don´t know what=
to do.
Should I just give selenium to try to minimize the damage or continue with=
a different
protocol to get the metals out? Should we continue to chelate or not? What=
would happen
if we do nothing, would her eyesight recover? She´s relatively high functi=
oning and would
hate to have her suffer damage on our efforts to get her better! I could no=
t forgive myself
if she goes blind on this!
Please advise. Thank you.
Patricia, mom to Lorena 5 ASD.
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