Re: autism and leukemia

[Guest guest]

Since I believe toxins and mercury are the cause of autism and cancer, I believe

that the longer a toxin stays in the body the chance of the body's cells are

going to mutate thus causing cancer, etc.. I really believe those that do not

show obvious signs of autism, ADHD, etc, are waiting in silence - I feel we will

have a cancer explosion in our young people.

Just my own view,

Kath

[Guest guest]

This raises a question regarding something someone told me recently.

This man had been dx'd with EBV about 15 years ago and was treated by

an alternative doctor who told him he felt there was a strong

connection between EBV and leukemia. Has anyone else heard this?

Michele

> Since I believe toxins and mercury are the cause of autism and

cancer, I believe that the longer a toxin stays in the body the

chance of the body's cells are going to mutate thus causing cancer,

etc.. I really believe those that do not show obvious signs of

autism, ADHD, etc, are waiting in silence - I feel we will have a

cancer explosion in our young people.

>

> Just my own view,

> Kath

[Guest guest]

I have an efriend here in UK, her Autistic son beat Leukemia at age 5 but

unfortunately died ealier this year from a brain tumour, he was 10

Mandi in UK

> My son has autism and had a brain tumor. I believe they were

> induced by a herpes virus and many other factors but I am sure the

> tumor came from a virus and Jack's autistic symptoms improved w/

> treatment of Valtrex.

>

> nne

>

> In , kahybl@a... wrote:

> >Since I believe toxins and mercury are the cause of autism and

> cancer, I believe that the longer a toxin stays in the body the

> chance of the body's cells are going to mutate thus causing cancer,

> etc.. I really believe those that do not show obvious signs of

> autism, ADHD, etc, are waiting in silence - I feel we will have a

>

[Guest guest]

--- In , " " <KRIVERA2@c...>

wrote:

> Hi all,

> I don't post very much but when I saw the topic I knew I needed

to, I have a dd who is recovered from autism, We used chelation and

numerous other therapies to get her where she is today, (She is now 8

years old),

> Recently we found out my son who is 2 (will be 3 Jan) has leukemia,

We beileve the leukemia was due mainly to exposure to high EMG from a

broken cable wire we were unaware of that wasin n our house from the

time he was 12 months until he was 18 months that was letting out very

HIGH amounts of EMGs,

> He however has never had any signs of PDD or any neurological issue.

He was never vaccinated, (we learned with my 1st child who was damaged

by them)

> Fyi, I also have a normal healthy 5 year old who has not had any

health issues.

> K

Dear K,

Please forgive me for offering a suggestion for your son when

you have not asked for it. I don't know -- sometimes people

don't ask because they think a condition is permanent and

can't be helped. Anyway, for any sort of cancer there are

several kinds of treatment worth considering--- at the top

of my list is ozone. This is helpful to different degrees

for different people and different kinds of cancer.

good wishes,

Moria

[Guest guest]

--- In , " " <KRIVERA2@c...>

wrote:

> Hi Moria,

> Actually I am on the oxy plus list too :-)

oh good, then you not only know about ozone, you also

got to read the recent discussion on cancer treatments

> We are using only " alternative " treatments with him right now.

Including ozone water, oil and saunas. Depending on his next blood

test we will start a more aggresive treatment, including Hulda 's

21 day treatment for incurable cancers.

> Alternative treatments + prayer cured my daughter of autism and I

beleive they will cure my son as well.

that is nice yeah!

Moria

[Guest guest]

,

I have been finding out that there is some common turf between autism and

leukemia in that in both conditions, there can be a failure to grow that

comes along with onset...not all the time, but in some. In leukemia, this

involves about 20% of patients, and in autism, I don't know, but the DAN

doctors told me that either failure to grow or gain weight or having

evidence of muscle wasting may effect more than 50%, and Dr. Wakefield has

shown growth charts at conferences showing slowed growth after the MMR and

again after the MMR booster that coincided with autistic regression.

Sometimes, the chemotherapy in leukemia (which also further slows growth)

can be so devastating to development that the child will develop

neurological problems or be frozen at one stage of development. I've

talked to a mother whose Downs child got leukemia and has autstic features

and I also know a child who is about fifteen and acts every bit like a

three year old, but had leukemia as a baby and was treated with chemotherapy.

But the possibility of a connection between issues in autism and leukemia

doesn't surprise me, really, because the brain and bone marrow have a lot

in common. When I was in graduate school and taking neuroscience courses,

old models had to yield to some new information that showed us

experimentally that the brain was continually making new cells and some of

those cells were migrating across the corpus callosum. There is an area of

the corpus callosum that seems thinner in autism, and it looked to me that

this was in the same area where the rat brain's new neurons were migrating.

What persuaded these cells to divide? Signals from the extracellular

matrix, and signals that were used to prod the " brain marrow " into

beginning to divide and create cells that would migrate. A flurry of

studies came out back then trying to figure out at what stage of

differentiation the cells that would divide this way would be found. What

they found is that you could take cells of this category and implant them

in the blood stream of an irradiated rat (just like before a bone marrow

transplant) and these neuron precursors would divide and start making the

full complement of blood cells. This discovery was very interesting to me

since as a teenager I experienced bone marrow failiure (aplastic anemia)

and in the year preceding that, I had a lot of trouble with schoolwork that

I had never experienced before. After learning of my hematological woes, I

was given steroids, and suddenly, I was making perfect grades and shocking

everybody with a reportcard of A plusses. Unfortunately, there were

horrible side effects, and soon the steroids failed to work and I ended up

in the hospital with a splenectomy. Back then they were not doing bone

marrow transplants.

Scientists also found that you could take blood cells and transplant them

to the brain and they would make glial cells, but it was hard to get them

to become neurons, if I am remembering right. This confirmed to me the

idea that the bone marrow and the brain marrow (the precursor cells to

neurons) may be vulnerable to the same influences.

Of course, since my " thing " is studying the sulfur chemistry, and since it

is clear that sulfur deficiencies will always lead to growth problems in

the very young, I am eager to see how close this resemblance may be.

As I've been studying this issue in the last months and as I've become

aware how important thiol/disulfide exchange is in the function of the

sulfur chemistry, I've realized that DMSA may help to speed up

thiol/disulfide exchange and recompartmentalize cysteine. This may get

growth started back again in some children who have enough sulfur stores in

their bodies to be able to tolerate the loss of the two cysteines that are

removed with every DMSA molecule they take in. Before getting to the

urine, that DMSA may have switched partners many times, accomplishing a lot

that a physiological thiol would normally do, so making up in part for a

slight sulfur deficiency, or a sulfur mistrafficking problem. This effect

is very similar to how economists talk about how people can use and spend

the same dollar many times and they can calculate how the velocity of the

way that dollar changes hands can add to the money supply in different

categories.

Anyway, it also seems clear that if you are at a serious stage of sulfur

depletion, DMSA might put you over the edge in a bad way, and it may do

that by taking cysteine out of places like bone marrow where it is not so

expendable. That is why it is very important to have the blood tests done

that are recommended in the PDR to ensure that you are not stressing the

bone marrow with DMSA. I've put an article below that found that DMSA was

surprisingly (uncharacteristically) found to seek out the bone marrow in a

child given DMSA to assess renal problems. Bad sulfur chemistry seems part

and parcel of most renal problems.

For these reasons, if you have leukemia in your family, I would think long

and hard before using DMSA or a similar drug for chelation, and would

consider using an approach that enhanced the supply of sulfur rather than

worked against it, but by all means, if you do use DMSA, follow the PDR

instructions on getting blood tests regularly.

Ann Nucl Med. 1993 Nov;7(4):281-3. Related Articles, Links

Increased bone marrow uptake on Tc-99m DMSA scintigraphy in a patient

with renal osteodystrophy.

Caglar M, Naldoken S.

Hacettepe University Faculty of Medicine, Department of Nuclear

Medicine, Ankara, Turkey.

A 16-year-old male patient was evaluated with Tc-99m

Diethylenetriamine-pentaacetic acid (DTPA) and Tc-99m 2-3

Dimercaptosuccinic acid (DMSA) scintigraphy for renal failure secondary to

renal calculi. The uptake in the renal cortex was significantly decreased

both on DMSA and DTPA studies. Uptake calculation on DMSA scintigraphy in

the kidneys disclosed values of less than 5%. The activity in the liver and

bone was significantly increased. A bone scan performed with Tc-99m

methylene diphosphonate (MDP) revealed increased bone uptake with decreased

soft tissue activity. Findings on bone scan were compatible with super

scan, most likely due to renal osteodystrophy. This case illustrates the

altered biodistribution of Tc-99m DMSA and a shift of the

radiopharmaceutical to the bone marrow which is not likely related to

colloid formation due to changes in mineral balance in patients with renal

failure.

Publication Types:

* Case Reports

PMID: 8292457 [PubMed - indexed for MEDLINE]

At 10:39 AM 12/30/2003 -0500, you wrote:

>A little girl in my son's class was just diagnosed with leukemia. I was

>wondering if there is any connection between vaccines, toxins and leukemia.

>karen

>

>

>

[Guest guest]

> >A little girl in my son's class was just diagnosed with leukemia.

I was

> >wondering if there is any connection between vaccines, toxins and

leukemia.

> >karen

> >

> >

> >

[Guest guest]

,

I'll get to your questions below, but I thought first I would put in the

warning that is in the PDR on blood problems with succimer. Unfortunately,

just like vaccines, the research into safety was very limited (as it says

in the PDR) and it didn't seem to look for long term issues.

The PDR is certainly likely to be assuming the dosage used for lead

poisoning, which is much higher than Andy recommends, but it is similar to

what was in the DAN! mercury consensus paper. The idea of long-term usage

of this product was not at all anticipated in the research that led to

DMSA's approval or in the guidelines in the PDR. I would recommend reading

the package insert to compare the use that was anticipated for the drug to

the use that is being employed in our circles.

-----------------------------------------------------

WARNINGS

Keep out of reach of pediatric patients. CHEMET is not a substitute for

effective abatement of lead exposure.

Mild to moderate neutropenia has been observed in some patients receiving

succimer. While a causal relationship to succimer has not been definitely

established, neutropenia has been reported with other drugs in the same

chemical class. A complete blood count with white blood cell differential

and direct platelet counts should be obtained prior to and weekly during

treatment with succimer. Therapy should either be withheld or discontinued

if the absolute neutrophil count (ANC) is below 1200/µL and the patient

followed closely to document recovery of the ANC to above 1500/µL or to the

patient's baseline neutrophil count. There is limited experience with

reexposure in patients who have developed neutropenia. Therefore, such

patients should be rechallenged only if the benefit of succimer therapy

clearly outweighs the potential risk of another episode of neutropenia and

then only with careful patient monitoring.

Patients treated with succimer should be instructed to promptly report any

signs of infection. If infection is suspected, the above laboratory tests

should be conducted immediately.

-----------------------------------------------------

It worries me that in the approval process, there seems to be a lack of

consideration of mechanisms that need to be tested. This other type of

research seems to be left to people doing studies AFTER the product is

already being used extensively.There was fairly recently a study funded by

the NIH that looked at giving high-dose DMSA while exposing pregnant rats

to mercury. They thought to look at the pups of a group that were exposed

to the DMSA but not the mercury, and found alterations in the immune system

in the pups that appeared to be permanent and showed up when they were

adults. I'll put that reference below, One of the people I talked to said

that he had talked to one of the authors of this study. The author had

wanted to further evaluate the risks of DMSA (and perhaps he would have

looked at lower doses) but he lost his funding and there was not much

chance it would be investigated further. Doesn't that sound typical?

How much investigation of potential long-term adverse reactions becomes

part of the approval process?

A number of years ago, having been exposed to the biological properties of

a chemical called PEG, I was shocked to learn that this drug had recent

approval as a treatment for constipation, and I learned how shortsighted

about mechanisms the approval process can be. I had learned about this

drug years before in graduate school where we studied about using this

compound to merge the membranes of cancer cells to normal cells in order to

give the normal cell the ability to survive in vitro that is typical of

cancer cells. There are thousands of articles on this process, and the

merging of DNA is almost instant with that product, but the outplaying of

the effect in producing cells with merged DNA was found in vitro to take

weeks or months to show up in changes in the cells. THIS part of the

mechanism was never investigated in the clinical trials, as all they

considered was whether it helped to relieve constipation, and just about

anything else that developed during the trial they deemed unrelated. So

this product is being given orally to people with terrible constipation, so

that it sits in the colon with a whole panoply of bacteria and fungi right

next to human cells, and the DNA of all these cells next to each other

would be expected to merge in unusual ways.

I am sorry that this " wait and see " is the way we do business in

pharmaceutical approvals. I may be a bit more sensitive to this issue since

my bone marrow failure was caused by taking an antibiotic that was

approved, but was being used by doctors inappropriately and without proper

followup. Most of the people who got the blood disease from this exposure

died, but it was a very rare reaction and didn't show up for many, many

months after you took the drug. This problem occurred in about one in

40,000 people who took the drug, so I obviously had some peculiar risk that

was quite rare. Is some of that risk the reason my child had developmental

delays? I don't know.

Neutropenia was part of my own set of blood problems. Does the literature

talk about any association between neutropenia (as can show up with DMSA)

and the later development of leukemia? Apparently, yes, sometimes. The

kicker here is that when there is a fragility in these cells, in other

conditions, they have found that a leukemic transformation might not occur

until many years later when children have become adults, as the second

article below mentioned. This just makes me aware that any drug you take

that may be associated with neutropenia may have unexpected risks. It is

possible that some of those risks may take even years to

manifest....something pharmaceutical companies just aren't going to address.

, you asked about what someone might use instead. There have

certainly been many discussions of alternatives on this list like ALA and

allithiamine which end up in a form of sulfur that is normal to the

body. Even though Andy doesn't approve of allithiamine, DAN! doctors have

described urinary tests that suggest that it is accomplishing the removal

of mercury regardless of its mechanism.

Keeping the sulfur chemistry nutritionally intact seems an appropriate

defense against environmental agents of all sorts that attack the sulfur

side of the chemistry, and an intact sulfur chemistry is protective against

effects of mercury exposure, and those with poor sulfur chemistry are the

ones who are most likely to be harmed by mercury, although they don't

necessarily end up with more in their bodies. It just is more harmful.

But , I would think if your child was one of the ones who developed any

sort of blood problems using DMSA that the problems with their blood may

need to get more attention than worries about chelating heavy metals, for

it may be that such a child has other issues of chemistry that are

associated with their developmental difficulties, and those may need more

direct attention. Children with ASD are not all alike, as we keep learning.

My impression is that chemical participants in thiol/disulfide exchange in

the lysosome make up the type of chemical that can mobilize the mercury

stuck there so that it can get out of the cell and be excreted. The

science has not gotten that specific on research into DMSA, though it seems

it should have. For instance, looking for such articles, I found 98

articles talking about mercury collecting in the lysosome, but there were

zero articles on DMSA and its function or effect in the lysosome where

sulfur-recycling from proteins occurs.

Rev Clin Exp Hematol. 2003 Mar;7(1):72-83. Links

Congenital neutropenias.

Zeidler C, Schwinzer B, Welte K.

Department for Pediatric Hematology/Oncology, Kinderklinik

Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, 30625 Hannover.

Zeidler.Cornelia@...

The term congenital neutropenia (CN) has been used for a group of

hematologic disorders characterized by severe neutropenia with absolute

neutrophil counts (ANC) below 0.5 x 10(9)/L associated with increased

susceptibility to bacterial infections. This group of diseases includes

primary bone marrow failure syndromes with isolated neutropenias and

neutropenias associated with metabolic or immunologic disorders or with a

complex syndrome. To avoid confusion, we prefer using the term CN only for

the most severe disorder among this group: severe neutropenia characterized

by an early stage maturation arrest of myelopoiesis leading to bacterial

infections from early infancy. This disease has originally been described

as Kostmann syndrome with an autosomal recessive inheritance. Recent

pathogenetic investigations have demonstrated that this clinical phenotype

includes also autosomal dominant and sporadic cases with different point

mutations in the neutrophil elastase gene in a subgroup of patients. Data

on over 400 patients with CN collected by the Severe Chronic Neutropenia

International Registry demonstrate that independent from the CN-subtype

more than 90% of these patients respond to recombinant human

granulocyte-colony stimulating factor (rHuG-CSF filgrastim, lenograstim)

with ANC that can be maintained around 1.0 x 10(9)/L. Adverse events

include mild splenomegaly, moderate thrombocytopenia, osteoporosis and

malignant transformation into myelodysplastic syndrome/leukemia.

Development of additional genetic aberrations, e.g., G-CSF-receptor gene

mutations, monosomy 7 or ras mutations during the course of the disease

indicate an underlying genetic instability leading to an increased risk of

malignant transformation. If and how G-CSF treatment impacts on these

adverse events remains unclear since there are no historical controls for

comparison. Hematopoietic stem cell transplantation is still the only

available treatment for patients refractory to G-CSF treatment.

PMID: 14692235 [PubMed - in process]

Eur J Haematol. 2003 Nov;71(5):393-5. Related Articles, Links

Shwachman-Diamond syndrome with late-onset neutropenia and fatal acute

myeloid leukaemia without maturation: a case report.

Lesesve JF, Dugue F, Gregoire MJ, Witz F, Dror Y.

Department of Biological Haematology, University Hospital, ,

France. jf.lesesve@...

We report on a male patient affected by Shwachman Diamond syndrome

(SDS) who presented an unusual delayed neutropenia and then developed a

poorly differentiated acute myeloid leukaemia (M0-AML) with trilineage

myelodysplasia in adulthood. Conventional cytogenetics revealed complex

karyotypic changes (monosomies 20, 21, 22, additional 15p). The patient was

treated with conventional chemotherapy but never reached complete remission

of leukaemia and died 18 months after diagnosis. SDS is an inherited bone

marrow failure syndrome with a high propensity to leukaemic transformation.

Since neutropenia may be intermittent or with delayed onset, and leukaemic

transformation may not occur until adulthood, full blood count should be

regularly monitored in such patients.

PMID: 14667205 [PubMed - in process]

Toxicol Appl Pharmacol. 1999 Oct 15;160(2):198-205. Related Articles, Links

[Click here to read]

Vicinal-thiol-containing molecules enhance but mono-thiol-containing

molecules reduce nickel-induced DNA strand breaks.

Lynn S, Yu GL, Yan K.

Institute of Zoology, Academia Sinica, Taipei, Taiwan, 11529, Republic

of China.

Several thiol-containing molecules (TCM) are currently used as

antidotes for nickel, and vicinal TCM seem to be more effective in

mobilizing tissue nickel than are mono TCM. Using single cell alkaline

electrophoresis, we have shown that the vicinal TCM, meso-2,

3-dimercaptosuccinic acid (DMSA), 2,3-dimercaptopropane-1-sulfonate, and

2,3-dimercaptopropanol markedly enhanced, whereas the mono TCM,

D-penicillamide, glutathione, beta-mercaptoethanol, and diethyl

dithiocarbomate, reduced nickel chloride (Ni)-induced DNA breaks in a human

leukemia cell line, NB4 cells. Ni or TCM alone did not induce plasmid DNA

breaks in test tubes and neither did Ni plus mono TCM; however, Ni plus

vicinal TCM did. Vicinal TCM did, but mono TCM did not generate H(2)O(2) in

solution. H(2)O(2) alone did not, but H(2)O(2) plus Ni induced plasmid DNA

breaks. Although Ni plus glutathione did not break DNA, Ni plus glutathione

plus H(2)O(2) did. The Ni-DMSA-induced DNA breaks in NB4 cells, as well as

in plasmids, were completely prevented by d-mannitol or partially prevented

by several antioxidants. Therefore, the DNA breaks induced by Ni plus

vicinal TCM seem to be due to the complex of Ni with TCM in concert with

the H(2)O(2) produced by the vicinal TCM. The results that DMSA at a

concentration as low as 5 microM enhanced the Ni-induced DNA breaks suggest

a further evaluation of the TCM as nickel chelators is needed. Copyright

1999 Academic Press.

PMID: 10527919 [PubMed - indexed for MEDLINE]

Toxicology. 1999 Jan 1;132(1):67-79. Related Articles, Links

[Click here to read]

Persistent effect of in utero meso-2,3-dimercaptosuccinic acid (DMSA)

on immune function and lead-induced immunotoxicity.

Chen S, Golemboski KA, FS, Dietert RR.

Institute for Comparative and Environmental Toxicology, Department of

Microbiology and Immunology, College of Veterinary Medicine, Cornell

University, Ithaca, NY 14853-6401, USA.

Meso-2,3-dimercaptosuccinic acid (DMSA) is a drug currently employed

for cheltion therapy in lead poisoning; however, little is known about its

potential effects on the immune system. To examine the effect of DMSA and

its capacity to reverse immunotoxicity resulting from exposure to lead in

utero, female Fischer 344 rats were administered lead acetate in drinking

water from 2 weeks prior to mating until parturition; DMSA was given by

gavage on days 6-21 of gestation. The immune function of the female

offspring was tested at 13 weeks of age. The results showed that lead (250

ppm) suppressed Th1-type responses (delayed-type hypersensitivity (DTH),

interferon gamma (IFN gamma) production), enhanced a Th2-type response

(interleukin-4 (IL-4) production), and increased tumor necrosis factor

alpha (TNF alpha) production from macrophages. DMSA treatment (60 mg/kg per

day) during pregnancy significantly lowered the blood lead levels of both

the embryos and the lactating dams as well as the milk lead level of

lactating dams. The chelation treatment also reversed the lead-induced

alterations in pup body weight, relative spleen weight, TNF alpha, and IL-4

production. But in utero exposure to DMSA alone resulted in decreased DTH

response in adult offspring. This was likely due to a reduced cell

recruitment, since plasma monocyte chemoattractant protein-1 (MCP-1) levels

were decreased. The DMSA-exposed offspring also demonstrated increased

interleukin-2 (IL-2) production. These results suggest that DMSA reverses

some of the lead-induced immunotoxicity; however, this treatment itself

during embryonic development produces subsequent adult immunomodulation.

PMID: 10199582 [PubMed - indexed for MEDLINE]

-

What kind of chelation would you recommended that enhanced the supply

of sulfur?> Also, which blood tests do you recommend for a child

using DMSA on a low dose, frequesnt schedule?

Your post was very intersting- even for a Poly Sci major who took

math for poets.

Thank you,

Robles