soy

[Guest guest]

Our Doctor. grow up in Korea and he sad he ate very

little soy. I am more concerned is the Round Up. If it

kills a plant you would not eat it, most farmer use

Round Up on Soy

--- <xander95608@...> wrote:

> I'm a soy eater, drink soy milk too. have been

> eating meat replacement gluten/soy foods since I was

> a kid... I also quit wearing a bra all day long for

> the past 5-6 years so my lymph ducts can flow with

> harmony.... Cancer does not run in my family. I

> just learned of the aluminum thing today. That

> might explain my memory problems. Both of my

> Chinese buddies are big time soy eaters and both

> nutty as fruitcakes. But I love them anyway.

> A lot of people have soy allergy. I might, I

> don't know why I break out in hives a lot. For sure

> Strawberries and chocolate.. maybe nectarines and

> possibly soy. I don't worry about it much, but the

> hives are annoying.

>

> fcunsrial@... wrote:

> Hi ,

> I agree that there are a number of problems with soy

> cultivation, GMO, mold, poor fermentation, etc. but

> I am referring not to the soy itself but the

> phytoestrogens textacts.

> The Japanese people eat lots of fermented soy

> products and I would not advise anyone to eat raw

> soy nuts but the phytoestrogens have been real

> lifesavers for many women who did not like the idea

> of putting synthetic estrogen into their bodies and

> have relied on soy phytoextarcs such as Denzein,

> Genistein, etc.

> Regards

> .

>

>

> ---------------------------------

> Stay in the know. Pulse on the new .com. Check

> it out.

>

> [Non-text portions of this message have been

> removed]

>

>

__________________________________________________

[Guest guest]

I gave #2 child 3 glasses of whole dairy milk and he fell asleep! He hadn't

had any for a couple of weeks. Maybe he has an intolerance as well???

_____

From:

[mailto: ] On Behalf Of Liz

Sent: Monday, June 25, 2007 1:53 PM

Subject: [ ] Soy

Hi there,

We put the family on GFCF a month ago and it has clearly helped all of

us each in a different way. It seems losing the wheat made son with

speech isue less irritable and losing the dairy improved hearing, speech

and bowels. We stayed away from soy because we heard it had a similar

opiate effect in kids who needed GFCF. I did give both kids a soy pizza

today to see if anyhting changes. What I noticed is son is sleepy, the

poop is looser, lighter in color and smells similar to the old milk

poop...like cheetos. Anyone have a similar reaction with soy?

We are staying away from it in the future it was just crazy to me that

that little bit could create such a stink.

Liz

[Guest guest]

,

Drunk on milk! (and past out) I wonder how they will check for 'impaired milk

driving' when our kids grow up?

Let me tell you the difference in my boy on milk and off of milk.

On milk = global developmental dyspraxia = slurs when he speaks, full of saliva

and drool, swallowing difficulties, trips, stumbles and falls, has trouble

following conversations, loss of sensation in his appendages (hands & feet,

lips, tongue), poor fine motor, poor gross motor, loss of balance, falls out of

his chair. Now a days, this happens within 1 - 2 hours of him consuming

anything with milk in it. A big sundae, he'll fall off his stool and be quite

deaf. A sandwich with casien in the bread, he lose language and have trouble

speaking.

Off of milk = normal little boy with a slight speech impediment (which is

getting better and better the longer he is off of milk); dysgraphia and other

slight fine motor issues. I believe if I had known about the milk issue before

he was 11; he would not suffer any speech issues or fine motor issues. I don't

know for sure but I do suspect it is the case.

Why is it so hard to believe that there could be a metabolic issue with milk?

Because we are taught that it is a wholesome product. Beer, wine, drugs affect

our neurological function and yet those who use those products are not labeled

with a 'psychiatric' diagnosis such as DSM-1V.

We should all collectively video tape our children before milk and after a big

sundae and send it to all of those doctors 'reading out of their textbooks' to

negate any ill affects at the vaccine trials. The collective evidence tells the

truth not some horned-rimmed scientist working from a petri-dish with an agenda

the size of Mount Olympus. What happened to listening to the parents anyway? I

am tired of doctors who roll their eyes and tell me to accept my childs

condition when I try to tell them what I am seeing. I am tired of being called

a 'hysterical mother' like some bad date who uses the 'crazy woman' defense to

handle rejection. Oh yeah, and PMS is all in my head too!

Believe me, I don't need a double-blinded, peer reviewed study to know the ill

affects on my boy! The longer milk is eliminated from his diet, the more

profoundly the differences. It now only takes a couple of hours for my child to

substantially lose his hearing after consuming milk. Milk products were

'stalling' his development and now that he is off of them for about 7 months

now, if he has any slip, his neurological processes are identical to that of

someone who is absolutely silly drunk! (not that I know about that)! Instead

of tossing his cookies into the toilet later on, he tosses his bowels.

Being off of milk is allowing my child to catch up neurodevelopmentally. It

still takes work because we have to go through the stages that he missed but he

is so 'normal' now. There are a few items but the prognosis is vastly different

than before. I know that he will go on to have a normal productive life if he

just keeps his lips off the milk carton. Oh, if only I had known when he was

2.... I could have prevented much of this tragedy.

Janice

My question is: What the heck is going on in the metabolism of all of our

children? We need the researchers to listen to us and to hear our collective

voice. How else are we to discover what other foods are damaging to our kids

and how are we to discover the changing nature of our human populous if we don't

seriously investigate this?

PS. Soy = milk with less intensity.

[ ] Soy

Hi there,

We put the family on GFCF a month ago and it has clearly helped all of

us each in a different way. It seems losing the wheat made son with

speech isue less irritable and losing the dairy improved hearing, speech

and bowels. We stayed away from soy because we heard it had a similar

opiate effect in kids who needed GFCF. I did give both kids a soy pizza

today to see if anyhting changes. What I noticed is son is sleepy, the

poop is looser, lighter in color and smells similar to the old milk

poop...like cheetos. Anyone have a similar reaction with soy?

We are staying away from it in the future it was just crazy to me that

that little bit could create such a stink.

Liz

[Guest guest]

Could be. If he does milk is literally like dope for him. My guy used to

do that.

Zeissler wrote:

>I gave #2 child 3 glasses of whole dairy milk and he fell asleep! He hadn't

>had any for a couple of weeks. Maybe he has an intolerance as well???

>

>

>

> _____

>

>From:

>[mailto: ] On Behalf Of Liz

>Sent: Monday, June 25, 2007 1:53 PM

>

>Subject: [ ] Soy

>

>

>

>Hi there,

>

>We put the family on GFCF a month ago and it has clearly helped all of

>us each in a different way. It seems losing the wheat made son with

>speech isue less irritable and losing the dairy improved hearing, speech

>and bowels. We stayed away from soy because we heard it had a similar

>opiate effect in kids who needed GFCF. I did give both kids a soy pizza

>today to see if anyhting changes. What I noticed is son is sleepy, the

>poop is looser, lighter in color and smells similar to the old milk

>poop...like cheetos. Anyone have a similar reaction with soy?

>

>We are staying away from it in the future it was just crazy to me that

>that little bit could create such a stink.

>

>

>Liz

>

>

>

>

>

>

[Guest guest]

I started my 19 month old apraxic son on a casein free diet 2 and a half weeks

ago. What I didn't realize the first week was that soy could have similar

effects as milk, so I did soy milk the first week and a half and then switched

to rice milk this week. I have noticed the last few days that my son is

starting to verbalize more. I have heard some words here and there, though they

come out so quickly I almost don't believe my ears. I find he is trying to

imitate my sounds more. I also feel he's been so interactive with great eye

contact this past week too....but I feel like this is crazy. Is it all in my

head? But I know I heard words! All I know is I'm sticking with the

casein-free diet and giving rice milk for a few more weeks. Who knows? Maybe

he's just developmentally ready, maybe it's the speech therapy, or maybe the

milk?!! I'm going to wait and see. Just wanted to share our latest

experiences.

Liz <lizlaw@...> wrote:

Hi there,

We put the family on GFCF a month ago and it has clearly helped all of

us each in a different way. It seems losing the wheat made son with

speech isue less irritable and losing the dairy improved hearing, speech

and bowels. We stayed away from soy because we heard it had a similar

opiate effect in kids who needed GFCF. I did give both kids a soy pizza

today to see if anyhting changes. What I noticed is son is sleepy, the

poop is looser, lighter in color and smells similar to the old milk

poop...like cheetos. Anyone have a similar reaction with soy?

We are staying away from it in the future it was just crazy to me that

that little bit could create such a stink.

Liz

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

Be a better Globetrotter. Get better travel answers from someone who knows.

Answers - Check it out.

[Guest guest]

I'd say it was the milk!

_____

From:

[mailto: ] On Behalf Of lauren baron

Sent: Monday, June 25, 2007 9:36 PM

Subject: Re: [ ] Soy

I started my 19 month old apraxic son on a casein free diet 2 and a half

weeks ago. What I didn't realize the first week was that soy could have

similar effects as milk, so I did soy milk the first week and a half and

then switched to rice milk this week. I have noticed the last few days that

my son is starting to verbalize more. I have heard some words here and

there, though they come out so quickly I almost don't believe my ears. I

find he is trying to imitate my sounds more. I also feel he's been so

interactive with great eye contact this past week too....but I feel like

this is crazy. Is it all in my head? But I know I heard words! All I know is

I'm sticking with the casein-free diet and giving rice milk for a few more

weeks. Who knows? Maybe he's just developmentally ready, maybe it's the

speech therapy, or maybe the milk?!! I'm going to wait and see. Just wanted

to share our latest experiences.

Liz <lizlawoptonline (DOT) <mailto:lizlaw%40optonline.net> net> wrote:

Hi there,

We put the family on GFCF a month ago and it has clearly helped all of

us each in a different way. It seems losing the wheat made son with

speech isue less irritable and losing the dairy improved hearing, speech

and bowels. We stayed away from soy because we heard it had a similar

opiate effect in kids who needed GFCF. I did give both kids a soy pizza

today to see if anyhting changes. What I noticed is son is sleepy, the

poop is looser, lighter in color and smells similar to the old milk

poop...like cheetos. Anyone have a similar reaction with soy?

We are staying away from it in the future it was just crazy to me that

that little bit could create such a stink.

Liz

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

Be a better Globetrotter. Get better travel answers from someone who knows.

Answers - Check it out.

[Guest guest]

Video tape him. Our video is broke. I know I saw lots of things and if

the therapists did not see it along with my husband I'd have nothing

left to do but check myself in somewhere for dementia.

lauren baron wrote:

>I started my 19 month old apraxic son on a casein free diet 2 and a half weeks

ago. What I didn't realize the first week was that soy could have similar

effects as milk, so I did soy milk the first week and a half and then switched

to rice milk this week. I have noticed the last few days that my son is

starting to verbalize more. I have heard some words here and there, though they

come out so quickly I almost don't believe my ears. I find he is trying to

imitate my sounds more. I also feel he's been so interactive with great eye

contact this past week too....but I feel like this is crazy. Is it all in my

head? But I know I heard words! All I know is I'm sticking with the

casein-free diet and giving rice milk for a few more weeks. Who knows? Maybe

he's just developmentally ready, maybe it's the speech therapy, or maybe the

milk?!! I'm going to wait and see. Just wanted to share our latest

experiences.

>

>

>Liz <lizlaw@...> wrote:

> Hi there,

>

>We put the family on GFCF a month ago and it has clearly helped all of

>us each in a different way. It seems losing the wheat made son with

>speech isue less irritable and losing the dairy improved hearing, speech

>and bowels. We stayed away from soy because we heard it had a similar

>opiate effect in kids who needed GFCF. I did give both kids a soy pizza

>today to see if anyhting changes. What I noticed is son is sleepy, the

>poop is looser, lighter in color and smells similar to the old milk

>poop...like cheetos. Anyone have a similar reaction with soy?

>

>We are staying away from it in the future it was just crazy to me that

>that little bit could create such a stink.

>

>

>Liz

>

>

>

>

>

>

>---------------------------------

>Be a better Globetrotter. Get better travel answers from someone who knows.

> Answers - Check it out.

>

>

[Guest guest]

My guy is two and this is the difference on and off milk:

On milk: hearing cuts in and out. He can hear on milk (according to the

hearing test it is perfect hearing) but he hears like he is underwater.

He is mellow, doped up and has motor planning issues. Also, drooling

with open mouth. Not all the time with the open mouth though...it

depends on amount of milk in his system. The drooling though is

literally turned on with milk. Also congestion and snoring.

Off milk: More prone to speak, better hearing and interaction with

others, more alert, less tantrums, no congestion or snoring.

We have been off milk minus one trial day of pizza for one month. I have

noticed in that month that he has virtually no tone issues and runs

arouns with blinding speed. He is also not much of the humpty dumpty kid

in the bucket swing anymore. I know therapy played a role but after

reading your story I truly believe that being off milk and staying off

has contrinuted to this as well. He has lost the nasal tone (it took 3

weeks) but still has articulation issues. I am not so sure that some of

that is not simply age though so time will likely tell the story.

I am not yet sure what gluten does to him other than irritability.

Things are going well so I won;t play with that for now.

Janice, the hope you give me is so awesome.

Liz

Janice wrote:

>,

>

>Drunk on milk! (and past out) I wonder how they will check for 'impaired milk

driving' when our kids grow up?

>

>Let me tell you the difference in my boy on milk and off of milk.

>

>On milk = global developmental dyspraxia = slurs when he speaks, full of saliva

and drool, swallowing difficulties, trips, stumbles and falls, has trouble

following conversations, loss of sensation in his appendages (hands & feet,

lips, tongue), poor fine motor, poor gross motor, loss of balance, falls out of

his chair. Now a days, this happens within 1 - 2 hours of him consuming

anything with milk in it. A big sundae, he'll fall off his stool and be quite

deaf. A sandwich with casien in the bread, he lose language and have trouble

speaking.

>

>Off of milk = normal little boy with a slight speech impediment (which is

getting better and better the longer he is off of milk); dysgraphia and other

slight fine motor issues. I believe if I had known about the milk issue before

he was 11; he would not suffer any speech issues or fine motor issues. I don't

know for sure but I do suspect it is the case.

>

>Why is it so hard to believe that there could be a metabolic issue with milk?

Because we are taught that it is a wholesome product. Beer, wine, drugs affect

our neurological function and yet those who use those products are not labeled

with a 'psychiatric' diagnosis such as DSM-1V.

>

>We should all collectively video tape our children before milk and after a big

sundae and send it to all of those doctors 'reading out of their textbooks' to

negate any ill affects at the vaccine trials. The collective evidence tells the

truth not some horned-rimmed scientist working from a petri-dish with an agenda

the size of Mount Olympus. What happened to listening to the parents anyway? I

am tired of doctors who roll their eyes and tell me to accept my childs

condition when I try to tell them what I am seeing. I am tired of being called

a 'hysterical mother' like some bad date who uses the 'crazy woman' defense to

handle rejection. Oh yeah, and PMS is all in my head too!

>

>Believe me, I don't need a double-blinded, peer reviewed study to know the ill

affects on my boy! The longer milk is eliminated from his diet, the more

profoundly the differences. It now only takes a couple of hours for my child to

substantially lose his hearing after consuming milk. Milk products were

'stalling' his development and now that he is off of them for about 7 months

now, if he has any slip, his neurological processes are identical to that of

someone who is absolutely silly drunk! (not that I know about that)! Instead

of tossing his cookies into the toilet later on, he tosses his bowels.

>

>Being off of milk is allowing my child to catch up neurodevelopmentally. It

still takes work because we have to go through the stages that he missed but he

is so 'normal' now. There are a few items but the prognosis is vastly different

than before. I know that he will go on to have a normal productive life if he

just keeps his lips off the milk carton. Oh, if only I had known when he was

2.... I could have prevented much of this tragedy.

>

>Janice

>

>

>My question is: What the heck is going on in the metabolism of all of our

children? We need the researchers to listen to us and to hear our collective

voice. How else are we to discover what other foods are damaging to our kids

and how are we to discover the changing nature of our human populous if we don't

seriously investigate this?

>

>

>PS. Soy = milk with less intensity.

>

>

> [ ] Soy

>

> Hi there,

>

> We put the family on GFCF a month ago and it has clearly helped all of

> us each in a different way. It seems losing the wheat made son with

> speech isue less irritable and losing the dairy improved hearing, speech

> and bowels. We stayed away from soy because we heard it had a similar

> opiate effect in kids who needed GFCF. I did give both kids a soy pizza

> today to see if anyhting changes. What I noticed is son is sleepy, the

> poop is looser, lighter in color and smells similar to the old milk

> poop...like cheetos. Anyone have a similar reaction with soy?

>

> We are staying away from it in the future it was just crazy to me that

> that little bit could create such a stink.

>

>

> Liz

>

>

[Guest guest]

Is it true that soy can also be a problem for kids with milk issues?

**************The year's hottest artists on the red carpet at the Grammy

Awards. Go to AOL Music.

(http://music.aol.com/grammys?NCID=aolcmp00300000002565)

[Guest guest]

,

Soy creates estrogen. It also wreaks havoic on the metabolic system. Just a

little tidbit on soy.

Colleen

Re: [ ] Re:soy

Is it true that soy can also be a problem for kids with milk issues?

**************The year's hottest artists on the red carpet at the Grammy

Awards. Go to AOL Music.

(http://music. <http://music.aol.com/grammys?NCID=aolcmp00300000002565>

aol.com/grammys?NCID=aolcmp00300000002565)

[Guest guest]

Some yes, some no. People say the chemical structure of milk, soy, and

gluten are all similar, and that's why some kids have problems with all

three. We have a definite problem with dairy, but not soy. That said,

most of the soy is also genetically modified and theoretically, that is

behind the increase in soy allergies. Also, soy is in so much

processed stuff these days that we are all exposed to it a lot more.

Also, there is a difference between soy protein and soy lecithin and

soybean oil. Apparently, more people are sensitive to the protein than

the other two. Which is good, because those two are way more common.

in NJ

>

> Is it true that soy can also be a problem for kids with milk issues?

>

>

>

> **************The year's hottest artists on the red carpet at the

Grammy

> Awards. Go to AOL Music.

> (http://music.aol.com/grammys?NCID=aolcmp00300000002565)

>

>

>

[Guest guest]

Well-- everyone really should be very careful with soy since it can cause

problems with the thyroid and hormone issues as a result.

Most people shy away from it due to that reason alone-- but I think that in

slight amounts it should be ok for a healthy child/adult

Becky

**************Ideas to please picky eaters. Watch video on AOL Living.

(http://living.aol.com/video/how-to-please-your-picky-eater/rachel-campos-duffy/

2050827?NCID=aolcmp00300000002598)

[Guest guest]

There are a couple of things with soy. The whole estrogen thing, the

fact that a lot of soy is, for lack of a better term, messed with, as

is corn these das, and I read today in IBD an article entitled:

A Heyday in the Hearland: Fertilizer makers profit as soybeans battle

corn for U.S. farm acreage.

I think that says it all:)

Somedays instead of saying how did this happen to these kids I think,

how could it not? They are literally canaries in the coal mine.

>

> ,

>

> Soy creates estrogen. It also wreaks havoic on the metabolic

system. Just a

> little tidbit on soy.

>

> Colleen

>

> Re: [ ] Re:soy

>

>

>

> Is it true that soy can also be a problem for kids with milk

issues?

>

> **************The year's hottest artists on the red carpet at the

Grammy

> Awards. Go to AOL Music.

> (http://music. <http://music.aol.com/grammys?

NCID=aolcmp00300000002565>

> aol.com/grammys?NCID=aolcmp00300000002565)

>

>

[Guest guest]

Are these problems with soy primarily from the soy protein?

in NJ

>

> Well-- everyone really should be very careful with soy since it

can cause

> problems with the thyroid and hormone issues as a result.

> Most people shy away from it due to that reason alone-- but I think

that in

> slight amounts it should be ok for a healthy child/adult

>

>

> Becky

>

>

>

> **************Ideas to please picky eaters. Watch video on AOL

Living.

> (http://living.aol.com/video/how-to-please-your-picky-eater/rachel-

campos-duffy/

> 2050827?NCID=aolcmp00300000002598)

>

>

>

[Guest guest]

Phytoestrogens - Immune System Effects

Reports in the scientific literature of the potential effects of soy

on immune system function have been numerous over the last five

years. In particular the ability of the soy phytoestrogen genistein

to inhibit tyrosine kinases is well documented. The slant of much of

the research into this aspect of soy has been toward the possible

role of genistein in fighting cancer, but Soy Online Service believes

the potential for soy cause immune system disorders has been

overlooked.

Just how might genistein affect immune system function? Genistein

has been described as a potent immunosuppressant.

Soy Online Service often receives reports of the association of

another auto-immune disease with soy consumption, both in adults and

in children who had been fed soy formulas as infants. That disease is

alopecia. Read the experience of such a victim here

http://members.aol.com/greentek/hairloss.html.

References

Excessive soy consumption has been linked to migraine pain. Read more

about this here.

An article published in Scientific American (2002) suggests soy

infant formula may impair the developing immune system. Read More

Here

The literature is replete with numerous studies showing deleterious

effects on multiple organ systems - including the immune system. For

example this letter from the American Journal of Clinical Nutrition.

Early exposure to genistein exerts long-lasting effects on the

endocrine and immune systems in rats.

Klein SL, Wisniewski AB, Marson AL, Glass GE, Gearhart JP.

Mol Med 2002 Nov;8(11):742-9

Discussion: These data illustrate that exposure to genistein during

pregnancy and lactation exerts long-lasting effects on the endocrine

and immune systems in adulthood. Whether exposure to phytoestrogens

during early development affects responses to infectious or

autoimmune diseases, as well as cancers, later in life requires

investigation.

Full Abstract Here

The phytoestrogen genistein induces thymic and immune changes: A

human health concern?

Srikanth Yellayi*, Afia Naaz*, A. Szewczykowski*, Tomomi

Sato*, A. Woods, Jongsoo Chang§, ngela Segre¶, Clint D.

Allred§, G. Helferich§,, and S. Cooke* Proc. Natl. Acad.

Sci. USA, Vol. 99, Issue 11, 7616-7621, May 28, 2002

Use of soy-based infant formulas and soy/isoflavone supplements has

aroused concern because of potential estrogenic effects of the soy

isoflavones genistein and daidzein.

....genistein produced suppression of humoral immunity.

Genistein injected at 8 mg/kg per day produced serum genistein levels

comparable to those reported in soy-fed human infants, and this dose

caused significant thymic and immune changes in mice.

Critically, dietary genistein at concentrations that produced serum

genistein levels substantially less than those in soy-fed infants

produced marked thymic atrophy. These results raise the possibility

that serum genistein concentrations found in soy-fed infants may be

capable of producing thymic and immune abnormalities, as suggested by

previous reports of immune impairments in soy-fed human infants.

Full Abstract Here

Breast feeding and insulin-dependent diabetes mellitus in children

Fort P. Lanes R. Dahlem S. Recker B. Weyman-Daum M. Pugliese M.

Lifshitz F.

Journal of the American College of Nutrition. 5(5):439-41, 1986.

Abstract

We have evaluated the hypothesis of a protective effect of human milk

on the development of insulin dependent diabetes mellitus (IDDM). We

studied the feeding histories of 95 diabetic children and compared

them with controls consisting of their non-diabetic siblings and a

pair matched group of nondiabetic peers of the same age, sex,

geographical location, and social background. The incidence of breast

feeding in diabetic children was 18%. This was similar to the control

group. The duration of breast feedings was also similar among all

three groups. There was no difference in the age of introduction of

solid food between diabetic and nondiabetic children. Twice as many

diabetic children, however, received soy containing formula in

infancy as compared to control children. The mean age of onset of

IDDM was not related to the type of feeding during infancy. The

incidence of positive thyroid antibodies was two and one half times

higher in formula-fed diabetic children than in breast-fed ones. In

our studies we were unable to document any relationship between the

history of breast feeding and subsequent development of IDDM in

children.

Breast and soy-formula feedings in early infancy and the prevalence

of autoimmune thyroid disease in children.

Fort P, Moses N, Fasano M, Goldberg T, Lifshitz F.

Department of Pediatrics, North Shore University Hospital-Cornell

University Medical College, Manhasset, New York 11030.

Am Coll Nutr 1990 Apr;9(2):164-7

Abstract

It has been suggested that feeding practices in infancy may affect

the development of various autoimmune diseases later in life. Since

thyroid alterations are among the most frequently encountered

autoimmune conditions in children, we studied whether breast and soy-

containing formula feedings in early life were associated with the

subsequent development of autoimmune thyroid disease. A detailed

history of feeding practices was obtained in 59 children with

autoimmune thyroid disease, their 76 healthy siblings, and 54 healthy

nonrelated control children. There was no difference in the frequency

and duration of breast feeding in early life among the three groups

of children. However, the frequency of feedings with soy-based milk

formulas in early life was significantly higher in children with

autoimmune thyroid disease (prevalence 31%) as compared with their

siblings (prevalence 12%; chi 2 = 7.22 with continuity factor; p less

than 0.01), and healthy nonrelated control children (prevalence 13%,

chi 2 = 5.03 with continuity factor; p less than 0.02). Therefore,

this retrospective analysis documents the association of soy formula

feedings in infancy and autoimmune thyroid disease.

Odd chromosome movement and inaccurate chromosome distribution in

mitosis and meiosis after treatment with protein kinase inhibitors.

Nicklas RB, Krawitz LE, Ward SC

J Cell Sci 1993 Apr 104 ( Pt 4) 961-73

Abstract

Errors in chromosome orientation in mitosis and meiosis are

inevitable, but normally they are quickly corrected. We find that

such errors usually are not corrected in cells treated with protein

kinase inhibitors. Highly inaccurate chromosome distribution is the

result. When grasshopper spermatocytes were treated with the kinase

inhibitor 6-dimethylaminopurine (DMAP), 84% of maloriented

chromosomes failed to reorient; in anaphase, both partner chromosomes

were distributed to the same daughter cell. These chromosomes were

observed for a total of over 60 h, and not a single reorientation was

seen. In contrast, in untreated cells, maloriented chromosomes

invariably reoriented, and quickly: in 10 min, on average. A second

protein kinase inhibitor, genistein, had exactly the same effect as

DMAP. DMAP affected PtK1 cells in mitosis as it did spermatocytes in

meiosis: improper chromosome orientations persisted, leading to

frequent errors in distribution. We micromanipulated chromosomes in

spermatocytes treated with DMAP to learn why maloriented chromosomes

often fail to reorient. Reorientation requires the loss of improper

microtubule attachments and the acquisition of new, properly directed

kinetochore microtubules. Micromanipulation experiments disclose that

neither the loss of old nor the acquisition of new microtubules is

sufficiently affected by DMAP to account for the indefinite

persistence of malorientations. Drug treatment causes a novel form of

chromosome movement in which one kinetochore moves toward another

kinetochore. Two kinetochores in the same chromosome or in different

chromosomes can participate, producing varied, dance-like movements

executed by one or two chromosomes. These kinetochore-kinetochore

interactions evidently are at the expense of kinetochore-spindle

interactions. We propose that malorientations persist in treated

cells because the kinetochores have numerous, short microtubules with

a free end that can be captured by a second kinetochore. Kinetochores

capture each other's kinetochore microtubules, leaving too few sites

available for the efficient capture of spindle microtubules. Since

the efficient capture of spindle microtubules is essential for the

correction of errors, failure of capture allows malorientations to

persist. Whether the effects of DMAP actually are due to protein

kinase inhibition remains to be seen. In any case, DMAP reveals

interactions of one kinetochore with another, which, though

ordinarily suppressed, have implications for normal mitosis.

Flavonoids as DNA topoisomerase antagonists and poisons: structure-

activity relationships.

Constantinou A, Mehta R, Runyan C, Rao K, Vaughan A, Moon R

J Nat Prod 1995 Feb 58:2 217-25

Abstract

Selected flavonoids were tested for their ability to inhibit the

catalytic activity of DNA topoisomerase (topo) I and II. Myricetin,

quercetin, fisetin, and morin were found to inhibit both enzymes,

while phloretin, kaempferol, and 4',6,7-trihydroxyisoflavone

inhibited topo II without inhibiting topo I. Flavonoids demonstrating

potent topo I and II inhibition required hydroxyl group substitution

at the C-3, C-7, C-3', and C-4' positions and also required a keto

group at C-4. Additional B-ring hydroxylation enhanced flavonoid topo

I inhibitory action. A C-2, C-3 double bond was also required, but

when the A ring is opened, the requirement for the double bond was

eliminated. Genistein has been previously reported to stabilize the

covalent topo II-DNA cleavage complex and thus function as a topo II

poison. All flavonoids were tested for their ability to stabilize the

cleavage complex between topo I or topo II and DNA. None of the

agents stabilized the topo I-DNA cleavage complex, but prunetin,

quercetin, kaempferol, and apigenin stabilized the topo II DNA-

complex. Competition experiments have shown that genistein-induced

topo II-mediated DNA cleavage can be inhibited by myricetin,

suggesting that both types of inhibitors (antagonists and poisons)

interact with the same functional domain of their target enzyme.

These results are of use for the selection of flavonoids that can

inhibit specific topoisomerases at specific stages of the

topoisomerization reaction.

Genistein as an inducer of tumor cell differentiation: possible

mechanisms of action.

Constantinou A, Huberman E

Proc Soc Exp Biol Med 1995 Jan 208:1 109-15

Abstract

Decreased activity of either topoisomerases or tyrosine kinases has

been implicated in the differentiation of a number of cell types. It

is therefore conceivable that genistein, because of its reported

ability to inhibit these activities in vitro, may be an inducer of

cellular differentiation. We investigated this possibility in human

promyelocytic HL-60 and erythroid K-562 leukemia cells and in human

SK-MEL-131 melanoma cells. Our results indicated that genistein, in a

dose-dependent manner, inhibited cell multiplication and induced cell

differentiation. The maturing HL-60 cells acquired granulocytic and

monocytic markers. The differentiating K-562 cells stained positively

with benzidine, which indicates the production of hemoglobin, an

erythroid marker. Following genistein treatment, maturing SK-MEL-131

melanoma cells formed dendrite-like structures and exhibited

increased tyrosinase activity and melanin content. Experiments were

designed to identify the molecular mechanism of genistein's action.

Data from our laboratory suggest that this isoflavone triggers the

pathway that leads to cellular differentiation by stabilizing protein-

linked DNA strand breakage. Other possible mechanisms reported in the

literature are discussed.

Genistein induces apoptosis in immature human thymocytes by

inhibiting topoisomerase-II.

McCabe MJ Jr, Orrenius S

Biochem Biophys Res Commun 1993 Jul 30 194:2 944-50

Abstract

The toxicity of genistein, an inhibitor of tyrosine kinases and

topoisomerase-II, on human thymocytes was investigated. Genistein

induced marked chromatin fragmentation indicative of apoptosis in

human thymocyte cultures. Genistein-induced thymocyte apoptosis is

unlikely due to an inhibition of basal tyrosine kinase activity,

since another tyrosine kinase inhibitor, herbimycin A, does not

induce thymocyte apoptosis, whereas other topoisomerase-II inhibitors

do. The thymocyte subpopulation most sensitive to genistein-induced

apoptosis exhibited a CD3-CD4+CD8+ phenotype. This subpopulation of

thymocytes is also sensitive to glucocorticoid-induced apoptosis;

however, differences between genistein- and glucocorticoid-induced

apoptosis were noted. In particular, unlike glucocorticoid-induced

apoptosis, genistein-induced apoptosis does not involve changes in

[Ca2+]i and cannot be blocked by activation of protein kinase C.

p53, mutations, and apoptosis in genistein-exposed human

lymphoblastoid cells.

SM, Chen JJ, Domon OE, McGarrity LJ, Bishop ME, Manjanatha MG,

Casciano DA

Mutat Res 1998 Aug 31 405:1 41-56

Abstract

The phytoestrogen, genistein, is a naturally occurring isoflavone

found in soy products. On a biochemical basis, genistein is a

competitive inhibitor of tyrosine kinases and the DNA synthesis-

related enzyme, topoisomerase-II (topo-II). Exposure of mammalian

cells to genistein results in DNA damage that is similar to that

induced by the topo-II inhibitor and chromosomal mutagen, m-amsa. In

order to determine the potential genotoxicity of genistein, human

lymphoblastoid cells which differ in the functional status of the

tumor suppressor gene, p53, were exposed to genistein and the

induction of micronuclei quantified by

microscopic analysis. In addition, the mutant fraction at the

thymidine kinase (tk) locus (both the normal-growth and slow-growth

phenotypes) was determined by resistance to trifluorothymidine (TFT)

and at the hypoxanthine phosphoribosyl transferase (hprt) locus by

resistance to 6-thioguanine (6-TG). Flow cytometric analysis of the

percentage of viable, apoptotic and degenerating cells was utilized

to determine the rate and kinetics of cell death after genistein

exposure. The detection of micronuclei in both cell lines indicated

that genistein-induced damage had occurred in both AHH-1 tk+/- and

L3. Linear regression analysis detected a significant increase in the

number of 6-TG-resistant clones in both AHH-1 tk+/- (p53+/-) and L3

(p53+/+). A comparison of slopes revealed no difference between the

lines. In contrast, a significant, concentration-dependent increase

in the number of TFT-resistant clones with the slow-growth phenotype

was detected in AHH-1 tk+/- (mutant p53), but not in L3 (wild-type

p53). Cell death occurred primarily by apoptosis in both cell lines;

however, a concentration-dependent decrease in the percentage of

viable cells was detected immediately after exposure in L3, but not

until 32 h after exposure in AHH-1 tk+/-. A comparison of the slopes

of the concentration-response curves for the percentage of viable

cells revealed no difference between the cell lines in the effect of

genistein on cell viability. Our results may be interpreted that

genistein is a chromosomal mutagen and that p53 functional status

affects the recovery of chromosomal mutants, possibly by signalling

cells into the apoptosis pathways.

Induction of mouse thymocyte apoptosis by inhibitors of tyrosine

kinases is associated with dephosphorylation of nuclear proteins.

Azuma Y, Onishi Y, Sato Y, Kizaki H

Cell Immunol 1993 Nov 152:1 271-8

Abstract

Incubation of mouse thymocytes with the protein tyrosine kinase

inhibitors herbimycin A and methyl-2,5-dihydroxycinnamate induced a

decreased and altered profile of nuclear phosphotyrosine proteins in

parallel with an increase in internucleosomal DNA fragmentation and

cell death dose-dependently. No change in the profile of cytoplasmic

phosphotyrosine proteins was observed. DNA fragmentation was

dependent on the synthesis of RNA and protein, suggesting that the

inhibition of tyrosine phosphorylation of the nuclear proteins

induces apoptosis. DNA fragmentation was enhanced by simultaneous

incubation with

phorbol esters capable of activating protein kinase C. Genistein,

another inhibitor of protein tyrosine kinase, induced DNA

fragmentation more rapidly than herbimycin A, but there was no

predominant alteration of phosphotyrosine proteins in early

incubation, suggesting that genistein may induce apoptosis by a

mechanism other than direct inhibition of protein tyrosinekinase

activity.

p53, mutations, and apoptosis in genistein-exposed human

lymphoblastoid cells.

SM, Chen JJ, Domon OE, McGarrity LJ, Bishop ME, Manjanatha MG,

Casciano DA.Mutat Res 1998 Aug 31;405(1):41-56

Our results may be interpreted that genistein is a chromosomal

mutagen ...

Full Abstract Here

[Guest guest]

Very interesting as my daughter has AA and soy was never a big part

of diet. No soy formula. Imagine if it was.

>

> Phytoestrogens - Immune System Effects

> Reports in the scientific literature of the potential effects of

soy

> on immune system function have been numerous over the last five

> years. In particular the ability of the soy phytoestrogen

genistein

> to inhibit tyrosine kinases is well documented. The slant of much

of

> the research into this aspect of soy has been toward the possible

> role of genistein in fighting cancer, but Soy Online Service

believes

> the potential for soy cause immune system disorders has been

> overlooked.

>

> Just how might genistein affect immune system function? Genistein

> has been described as a potent immunosuppressant.

>

> Soy Online Service often receives reports of the association of

> another auto-immune disease with soy consumption, both in adults

and

> in children who had been fed soy formulas as infants. That disease

is

> alopecia. Read the experience of such a victim here

> http://members.aol.com/greentek/hairloss.html.

>

>

>

> References

>

> Excessive soy consumption has been linked to migraine pain. Read

more

> about this here.

>

> An article published in Scientific American (2002) suggests soy

> infant formula may impair the developing immune system. Read More

> Here

>

> The literature is replete with numerous studies showing deleterious

> effects on multiple organ systems - including the immune system.

For

> example this letter from the American Journal of Clinical Nutrition.

>

>

>

> Early exposure to genistein exerts long-lasting effects on the

> endocrine and immune systems in rats.

> Klein SL, Wisniewski AB, Marson AL, Glass GE, Gearhart JP.

> Mol Med 2002 Nov;8(11):742-9

> Discussion: These data illustrate that exposure to genistein during

> pregnancy and lactation exerts long-lasting effects on the

endocrine

> and immune systems in adulthood. Whether exposure to phytoestrogens

> during early development affects responses to infectious or

> autoimmune diseases, as well as cancers, later in life requires

> investigation.

>

> Full Abstract Here

>

>

>

> The phytoestrogen genistein induces thymic and immune changes: A

> human health concern?

> Srikanth Yellayi*, Afia Naaz*, A. Szewczykowski*, Tomomi

> Sato*, A. Woods, Jongsoo Chang§, ngela Segre¶, Clint

D.

> Allred§, G. Helferich§,, and S. Cooke* Proc. Natl.

Acad.

> Sci. USA, Vol. 99, Issue 11, 7616-7621, May 28, 2002

> Use of soy-based infant formulas and soy/isoflavone supplements has

> aroused concern because of potential estrogenic effects of the soy

> isoflavones genistein and daidzein.

>

> ...genistein produced suppression of humoral immunity.

>

> Genistein injected at 8 mg/kg per day produced serum genistein

levels

> comparable to those reported in soy-fed human infants, and this

dose

> caused significant thymic and immune changes in mice.

>

> Critically, dietary genistein at concentrations that produced serum

> genistein levels substantially less than those in soy-fed infants

> produced marked thymic atrophy. These results raise the possibility

> that serum genistein concentrations found in soy-fed infants may be

> capable of producing thymic and immune abnormalities, as suggested

by

> previous reports of immune impairments in soy-fed human infants.

>

> Full Abstract Here

>

>

>

>

>

> Breast feeding and insulin-dependent diabetes mellitus in children

> Fort P. Lanes R. Dahlem S. Recker B. Weyman-Daum M. Pugliese M.

> Lifshitz F.

> Journal of the American College of Nutrition. 5(5):439-41, 1986.

> Abstract

> We have evaluated the hypothesis of a protective effect of human

milk

> on the development of insulin dependent diabetes mellitus (IDDM).

We

> studied the feeding histories of 95 diabetic children and compared

> them with controls consisting of their non-diabetic siblings and a

> pair matched group of nondiabetic peers of the same age, sex,

> geographical location, and social background. The incidence of

breast

> feeding in diabetic children was 18%. This was similar to the

control

> group. The duration of breast feedings was also similar among all

> three groups. There was no difference in the age of introduction of

> solid food between diabetic and nondiabetic children. Twice as many

> diabetic children, however, received soy containing formula in

> infancy as compared to control children. The mean age of onset of

> IDDM was not related to the type of feeding during infancy. The

> incidence of positive thyroid antibodies was two and one half times

> higher in formula-fed diabetic children than in breast-fed ones. In

> our studies we were unable to document any relationship between the

> history of breast feeding and subsequent development of IDDM in

> children.

>

>

> Breast and soy-formula feedings in early infancy and the prevalence

> of autoimmune thyroid disease in children.

> Fort P, Moses N, Fasano M, Goldberg T, Lifshitz F.

> Department of Pediatrics, North Shore University Hospital-Cornell

> University Medical College, Manhasset, New York 11030.

> Am Coll Nutr 1990 Apr;9(2):164-7

> Abstract

> It has been suggested that feeding practices in infancy may affect

> the development of various autoimmune diseases later in life. Since

> thyroid alterations are among the most frequently encountered

> autoimmune conditions in children, we studied whether breast and

soy-

> containing formula feedings in early life were associated with the

> subsequent development of autoimmune thyroid disease. A detailed

> history of feeding practices was obtained in 59 children with

> autoimmune thyroid disease, their 76 healthy siblings, and 54

healthy

> nonrelated control children. There was no difference in the

frequency

> and duration of breast feeding in early life among the three groups

> of children. However, the frequency of feedings with soy-based milk

> formulas in early life was significantly higher in children with

> autoimmune thyroid disease (prevalence 31%) as compared with their

> siblings (prevalence 12%; chi 2 = 7.22 with continuity factor; p

less

> than 0.01), and healthy nonrelated control children (prevalence

13%,

> chi 2 = 5.03 with continuity factor; p less than 0.02). Therefore,

> this retrospective analysis documents the association of soy

formula

> feedings in infancy and autoimmune thyroid disease.

>

>

> Odd chromosome movement and inaccurate chromosome distribution in

> mitosis and meiosis after treatment with protein kinase inhibitors.

> Nicklas RB, Krawitz LE, Ward SC

> J Cell Sci 1993 Apr 104 ( Pt 4) 961-73

> Abstract

> Errors in chromosome orientation in mitosis and meiosis are

> inevitable, but normally they are quickly corrected. We find that

> such errors usually are not corrected in cells treated with protein

> kinase inhibitors. Highly inaccurate chromosome distribution is the

> result. When grasshopper spermatocytes were treated with the kinase

> inhibitor 6-dimethylaminopurine (DMAP), 84% of maloriented

> chromosomes failed to reorient; in anaphase, both partner

chromosomes

> were distributed to the same daughter cell. These chromosomes were

> observed for a total of over 60 h, and not a single reorientation

was

> seen. In contrast, in untreated cells, maloriented chromosomes

> invariably reoriented, and quickly: in 10 min, on average. A second

> protein kinase inhibitor, genistein, had exactly the same effect as

> DMAP. DMAP affected PtK1 cells in mitosis as it did spermatocytes

in

> meiosis: improper chromosome orientations persisted, leading to

> frequent errors in distribution. We micromanipulated chromosomes in

> spermatocytes treated with DMAP to learn why maloriented

chromosomes

> often fail to reorient. Reorientation requires the loss of improper

> microtubule attachments and the acquisition of new, properly

directed

> kinetochore microtubules. Micromanipulation experiments disclose

that

> neither the loss of old nor the acquisition of new microtubules is

> sufficiently affected by DMAP to account for the indefinite

> persistence of malorientations. Drug treatment causes a novel form

of

> chromosome movement in which one kinetochore moves toward another

> kinetochore. Two kinetochores in the same chromosome or in

different

> chromosomes can participate, producing varied, dance-like movements

> executed by one or two chromosomes. These kinetochore-kinetochore

> interactions evidently are at the expense of kinetochore-spindle

> interactions. We propose that malorientations persist in treated

> cells because the kinetochores have numerous, short microtubules

with

> a free end that can be captured by a second kinetochore.

Kinetochores

> capture each other's kinetochore microtubules, leaving too few

sites

> available for the efficient capture of spindle microtubules. Since

> the efficient capture of spindle microtubules is essential for the

> correction of errors, failure of capture allows malorientations to

> persist. Whether the effects of DMAP actually are due to protein

> kinase inhibition remains to be seen. In any case, DMAP reveals

> interactions of one kinetochore with another, which, though

> ordinarily suppressed, have implications for normal mitosis.

>

> Flavonoids as DNA topoisomerase antagonists and poisons: structure-

> activity relationships.

> Constantinou A, Mehta R, Runyan C, Rao K, Vaughan A, Moon R

> J Nat Prod 1995 Feb 58:2 217-25

> Abstract

> Selected flavonoids were tested for their ability to inhibit the

> catalytic activity of DNA topoisomerase (topo) I and II. Myricetin,

> quercetin, fisetin, and morin were found to inhibit both enzymes,

> while phloretin, kaempferol, and 4',6,7-trihydroxyisoflavone

> inhibited topo II without inhibiting topo I. Flavonoids

demonstrating

> potent topo I and II inhibition required hydroxyl group

substitution

> at the C-3, C-7, C-3', and C-4' positions and also required a keto

> group at C-4. Additional B-ring hydroxylation enhanced flavonoid

topo

> I inhibitory action. A C-2, C-3 double bond was also required, but

> when the A ring is opened, the requirement for the double bond was

> eliminated. Genistein has been previously reported to stabilize the

> covalent topo II-DNA cleavage complex and thus function as a topo

II

> poison. All flavonoids were tested for their ability to stabilize

the

> cleavage complex between topo I or topo II and DNA. None of the

> agents stabilized the topo I-DNA cleavage complex, but prunetin,

> quercetin, kaempferol, and apigenin stabilized the topo II DNA-

> complex. Competition experiments have shown that genistein-induced

> topo II-mediated DNA cleavage can be inhibited by myricetin,

> suggesting that both types of inhibitors (antagonists and poisons)

> interact with the same functional domain of their target enzyme.

> These results are of use for the selection of flavonoids that can

> inhibit specific topoisomerases at specific stages of the

> topoisomerization reaction.

>

>

> Genistein as an inducer of tumor cell differentiation: possible

> mechanisms of action.

>

> Constantinou A, Huberman E

> Proc Soc Exp Biol Med 1995 Jan 208:1 109-15

> Abstract

> Decreased activity of either topoisomerases or tyrosine kinases has

> been implicated in the differentiation of a number of cell types.

It

> is therefore conceivable that genistein, because of its reported

> ability to inhibit these activities in vitro, may be an inducer of

> cellular differentiation. We investigated this possibility in human

> promyelocytic HL-60 and erythroid K-562 leukemia cells and in human

> SK-MEL-131 melanoma cells. Our results indicated that genistein, in

a

> dose-dependent manner, inhibited cell multiplication and induced

cell

> differentiation. The maturing HL-60 cells acquired granulocytic and

> monocytic markers. The differentiating K-562 cells stained

positively

> with benzidine, which indicates the production of hemoglobin, an

> erythroid marker. Following genistein treatment, maturing SK-MEL-

131

> melanoma cells formed dendrite-like structures and exhibited

> increased tyrosinase activity and melanin content. Experiments were

> designed to identify the molecular mechanism of genistein's action.

> Data from our laboratory suggest that this isoflavone triggers the

> pathway that leads to cellular differentiation by stabilizing

protein-

> linked DNA strand breakage. Other possible mechanisms reported in

the

> literature are discussed.

>

>

> Genistein induces apoptosis in immature human thymocytes by

> inhibiting topoisomerase-II.

> McCabe MJ Jr, Orrenius S

> Biochem Biophys Res Commun 1993 Jul 30 194:2 944-50

> Abstract

> The toxicity of genistein, an inhibitor of tyrosine kinases and

> topoisomerase-II, on human thymocytes was investigated. Genistein

> induced marked chromatin fragmentation indicative of apoptosis in

> human thymocyte cultures. Genistein-induced thymocyte apoptosis is

> unlikely due to an inhibition of basal tyrosine kinase activity,

> since another tyrosine kinase inhibitor, herbimycin A, does not

> induce thymocyte apoptosis, whereas other topoisomerase-II

inhibitors

> do. The thymocyte subpopulation most sensitive to genistein-induced

> apoptosis exhibited a CD3-CD4+CD8+ phenotype. This subpopulation of

> thymocytes is also sensitive to glucocorticoid-induced apoptosis;

> however, differences between genistein- and glucocorticoid-induced

> apoptosis were noted. In particular, unlike glucocorticoid-induced

> apoptosis, genistein-induced apoptosis does not involve changes in

> [Ca2+]i and cannot be blocked by activation of protein kinase C.

>

>

> p53, mutations, and apoptosis in genistein-exposed human

> lymphoblastoid cells.

> SM, Chen JJ, Domon OE, McGarrity LJ, Bishop ME, Manjanatha

MG,

> Casciano DA

> Mutat Res 1998 Aug 31 405:1 41-56

> Abstract

> The phytoestrogen, genistein, is a naturally occurring isoflavone

> found in soy products. On a biochemical basis, genistein is a

> competitive inhibitor of tyrosine kinases and the DNA synthesis-

> related enzyme, topoisomerase-II (topo-II). Exposure of mammalian

> cells to genistein results in DNA damage that is similar to that

> induced by the topo-II inhibitor and chromosomal mutagen, m-amsa.

In

> order to determine the potential genotoxicity of genistein, human

> lymphoblastoid cells which differ in the functional status of the

> tumor suppressor gene, p53, were exposed to genistein and the

> induction of micronuclei quantified by

> microscopic analysis. In addition, the mutant fraction at the

> thymidine kinase (tk) locus (both the normal-growth and slow-growth

> phenotypes) was determined by resistance to trifluorothymidine

(TFT)

> and at the hypoxanthine phosphoribosyl transferase (hprt) locus by

> resistance to 6-thioguanine (6-TG). Flow cytometric analysis of the

> percentage of viable, apoptotic and degenerating cells was utilized

> to determine the rate and kinetics of cell death after genistein

> exposure. The detection of micronuclei in both cell lines indicated

> that genistein-induced damage had occurred in both AHH-1 tk+/- and

> L3. Linear regression analysis detected a significant increase in

the

> number of 6-TG-resistant clones in both AHH-1 tk+/- (p53+/-) and L3

> (p53+/+). A comparison of slopes revealed no difference between the

> lines. In contrast, a significant, concentration-dependent increase

> in the number of TFT-resistant clones with the slow-growth

phenotype

> was detected in AHH-1 tk+/- (mutant p53), but not in L3 (wild-type

> p53). Cell death occurred primarily by apoptosis in both cell

lines;

> however, a concentration-dependent decrease in the percentage of

> viable cells was detected immediately after exposure in L3, but not

> until 32 h after exposure in AHH-1 tk+/-. A comparison of the

slopes

> of the concentration-response curves for the percentage of viable

> cells revealed no difference between the cell lines in the effect

of

> genistein on cell viability. Our results may be interpreted that

> genistein is a chromosomal mutagen and that p53 functional status

> affects the recovery of chromosomal mutants, possibly by signalling

> cells into the apoptosis pathways.

>

>

>

> Induction of mouse thymocyte apoptosis by inhibitors of tyrosine

> kinases is associated with dephosphorylation of nuclear proteins.

> Azuma Y, Onishi Y, Sato Y, Kizaki H

> Cell Immunol 1993 Nov 152:1 271-8

> Abstract

> Incubation of mouse thymocytes with the protein tyrosine kinase

> inhibitors herbimycin A and methyl-2,5-dihydroxycinnamate induced a

> decreased and altered profile of nuclear phosphotyrosine proteins

in

> parallel with an increase in internucleosomal DNA fragmentation and

> cell death dose-dependently. No change in the profile of

cytoplasmic

> phosphotyrosine proteins was observed. DNA fragmentation was

> dependent on the synthesis of RNA and protein, suggesting that the

> inhibition of tyrosine phosphorylation of the nuclear proteins

> induces apoptosis. DNA fragmentation was enhanced by simultaneous

> incubation with

> phorbol esters capable of activating protein kinase C. Genistein,

> another inhibitor of protein tyrosine kinase, induced DNA

> fragmentation more rapidly than herbimycin A, but there was no

> predominant alteration of phosphotyrosine proteins in early

> incubation, suggesting that genistein may induce apoptosis by a

> mechanism other than direct inhibition of protein tyrosinekinase

> activity.

>

>

> p53, mutations, and apoptosis in genistein-exposed human

> lymphoblastoid cells.

>

> SM, Chen JJ, Domon OE, McGarrity LJ, Bishop ME, Manjanatha

MG,

> Casciano DA.Mutat Res 1998 Aug 31;405(1):41-56

>

> Our results may be interpreted that genistein is a chromosomal

> mutagen ...

>

> Full Abstract Here

>

[Guest guest]

wezzie1954 writes:

> Whenever you have Cancer you need to stay away from soy

> products, because they will actually make the cancer grow more.

>

Best to stay away even if you don't have cancer, except for fermented soy.

[Guest guest]

The problem seems to be with estogen feed cancers tha soy mimics .However

fermented soy like tofu don't seem to carry yhe same risk

Joe turtle

Weston wrote:

" hariatmayoga " wrote:

> Whenever you have Cancer you need to stay away from soy

> products, because they will actually make the cancer grow more.

Now you've got me worried, I've used soya quite a lot as a substitute

for meat. If soya is bad, what's the situation with Quorn and Tofu?

[Guest guest]

greatyoga@... writes:

> I realize that but these things still help digest the soy, which is

> hard to digest.

>

Are you sure you want soy interfering with your estrogen?

[Guest guest]



Hahahaha, Katy you made me laugh with that one! Avoid a topic?! Bring it on.........the majority of people are so brainwashed by doctors, pharmacon, government, people with letters after their names (PhD, MD, DDS, RN, etc...), the internet, anything but listening to their own body. Ever watch a baby the first time it eats cereal? Spits it out! The baby knows that is not what should go down their gullet. It should be ripe, juicy fruits as their main food (well actually mother's milk, but.....)

Soy is one of the products that I avoid at all costs because it makes me feel weird, spacey, bloated, ick....even organic.

Shari

[Guest guest]

Actually, I was involved with people who consider soy to be a health food, I just couldn't hang with them anymore [these were real flesh and blood people, not a group] you know what I mean. And they ate so much of it. Maybe in Japan it's healthy where they only eat fermented soy and only about a teaspoon or so a day. I had been really sick for a month; healed up all by myself [health! what a concept] and I ate some soy oil cheese and got sick all over again for another 6 months, NO MORE SOY for this lil red hen! I don't see doctors regularly if I can avoid them. I'm NOT indoctrinated nor intiminated by the Alphabet people, they are just people who have been brainwashed by other brainwashed people with even more alphabet soup behind their names. Well that's my story and I'm sticking with it.

   ~Katy

Sheep to the right; His Lamb

Zeal for your house consumes me-Ps 69:9

http://orchardhouseheirlooms.com/product_info.php/cPath/157_163/products_id/199 survival seeds

Christian-homesteaders/?yguid=227010598 biblical survival

-- soy

 Hahahaha, Katy you made me laugh with that one! Avoid a topic?! Bring it on.........the majority of people are so brainwashed by doctors, pharmacon, government, people with letters after their names (PhD, MD, DDS, RN, etc...), the internet, anything but listening to their own body. Ever watch a baby the first time it eats cereal? Spits it out! The baby knows that is not what should go down their gullet. It should be ripe, juicy fruits as their main food (well actually mother's milk, but.....)

Soy is one of the products that I avoid at all costs because it makes me feel weird, spacey, bloated, ick....even organic.

Shari

[Guest guest]

Like most Asians I only consume very small quantities of soy...as a condiment.

There is so much hype about soy. here are a couple of links to get folks

thinking if they really want soy in their diet.

Be Well, Vicki

http://www.naturalhealthstrategies.com/dangers-of-soy.html

http://www.whale.to/a/soy2.html

[Guest guest]

>

> Like most Asians I only consume very small quantities of soy...as a condiment.

I try to tell people this all the time. But as Americans, I guess they have a

very warped sense of what the Asians are eating. I try to get Americans to

understand that we need to also look at what people AREN'T eating before

determing that something they ARE eating is the key to lower cancer risks.

ar

[Guest guest]

Genistein, the other isoflavones, and phytic acid (IP6) in soy are

cancer-healing, but nonfermented soy contains several genuinely harmful

ingredients.

>why it has to be fermented?

Fermented soy has enormously more genistein, and fermentation removes many of

soy's harmful ingredients.

For prevention, it's best to eat only modest amounts of (organic fermented) soy,

but to treat cancer, large amounts of (organic fermented) soy products are

needed (and are highly effective).

For more info on the negative aspects of soy (particularly nonfermented),

www.soyonlineservice.co.nz

http://articles.mercola.com/sites/articles/archive/2001/02/07/soy-heart-disease.\

aspx (Finucan & Charlotte Gerson)

http://www.mercola.com/article/soy/index.htm

www.mercola.com/article/soy/avoid_soy.htm (Fallon & Enig, Nexus magazine, 2000)

www.prostate90.com/sci_papers/soy_dangers.htm (Fallon & Enig, Nexus magazine,

2000)

Unfortunately, most people's views on soy are polarized, and extremist articles

on each side contain tons of misinformation.