A segueway into tylenol and medicines for respiratory infections

[Guest guest]

,

You asked:

>Does this mean that if I give my hfa son,(6 yrs old), guaifenisen syrup when

>he has respiratory mucus that I want to loosen and have him expel that it

>can cause problems for him by not getting to the lungs?

No, the issue I was presenting is that those with sulfation problems may

end up with TOO much of a dose getting to other organ systems, because an

inappropriately LOW amount of the dose is being disabled in the

gut Prescribed dosages are assuming that a certain amount of the drug

will be processed and disabled in the gut before it ever gets out into the

bloodstream. The dosages are set assuming that process is occurring

normally and will create a blood level within a certain expected range.

I don't know how guafenisen specifically is metabolized, but it is not on

the obvious " bad guy " list as far as demands on the sulfation

chemistry. Some medicines used for sore throats are phenols and say so and

are probably best avoided (like the throat sprays). I know with my

daughter, guafenisen is the cough syrup that seems to work the best.

I'd really like to thank Valentina for mentioning the mucolitic (mucolytic)

properties of NAC, for I chased that yesterday, and found out that NAC has

a long and successful history of being helpful in all sorts of respiratory

situations where there is too much or too " globby " mucus, including

asthma. " Lytic " is a root word that means " breaking something apart " , so

it may be doing the same sort of thing as guafenisin. What a great thing to

find out. I'm really curious about what actually changes, since mucins,

the proteins of mucus, are usually highly sulfated, and sulfated GAGs are

also released from mucus tissues during infection. I wonder if the

mucus becomes less sulfated as it becomes " globbier " ..,you know, that

awful stage when it isn't liquidy any more, and keeps tickling and making

you cough. That stage can last so long after the feeling of being sick is

gone.

Since it seems the sulfate chemistry is sort of put on hold during the main

part of infection, it would seem reasonable to think the end result of

infection might be less sulfate in the mucus...but I'd love to know for sure.

Dr. Waring found out in the laboratory that TNF, an immune factor turned on

during inflammation, suppressed the conversion of cysteine to sulfate in

neurons and GI tract cells. That makes it very interesting to think about

what might be happening with sulfation during this sort of dose of NAC used

for its mucolytic properties. I don't know about mucins particularly, but

with sulfated GAGs, the enzymes that break them apart are looking for a

certain pattern of sulfate to tell the enzyme where to clip the chain in

half. So it may be that adding cysteine at this time helps properly

resulfate these proteins and provide the " key " to breaking up the

" leftovers " .

TPST, the enzyme that sulfates mucins, was measured in autism by Dr.

Waring, and found to be suppressed in activity: in some children almost

completely. One thing that is puzzling about her finding on TNF

suppressing the enzyme that converts cysteine to the first step on the way

to sulfate is that those with AIDS, who of course have horrible problems

with inflammation and too much immune activation, do very well with NAC,

especially in helping to resolve the immune problems that seem to happen as

a result of low sulfur...things like poor natural killer cell activity and

poor T cell cytotoxicity, things that make it hard to keep from getting

sick after an exposure to a disease.

Some children with autism react negatively in a very obvious way to NAC,

but for those who can process it effectively, there is a reason to suspect

it may supply a double benefit during times when there is a respiratory

problem. I had wondered about what it would do for " sinus headaches " , and

was glad to see there was an old unabstracted article about that I've put

below.

Anyway, I've put an example of the NAC/mucolytic articles below. I am very

in favor of finding treatments that WORK, but which don't further strain

the sulfation chemistry.

Pretty much all pain killers strain the sulfate chemistry, but some more

than others. Aspirin and tylenol are BAD in this way. Motrin is sort of

in the middle, and naproxen sodium (naprosyn) seems to put the least strain

on sulfation. I hadn't really heard of naprosyn being used or marketed for

use in children, and wondered why that was, but I did find in the

literature that it is used for children with conditions of chronic pain

like arthritis. So, maybe after the holidays I can make an inquiry with

the manufacturer and get the scoop on whether it is considered safe for

children in other situations. I also know parents whose children, like

mine, don't seem to get any benefit from tylenol anyway. We use motrin,

but only when absolutely necessary and often in half-doses.

I hope this was practical enough for you, . I do the research side,

and am not a doctor, so I'll probably always be more focused on the whys

than the whats, but of course, all of this has to boil down to the " what to

do's " eventually!

Fortschr Med 1992 Jun 30;110(18):346-50

[Therapy of respiratory tract diseases with N-acetylcysteine. An open

therapeutic observation study of 2,512 patients]

[Article in German]

Volkl KP, Schneider B.

Institut fur Biometrie der Med. Hochschule Hannover.

STUDY DESIGN: Open therapeutic observational study. PATIENTS: 2,510 patients

with acute and chronic bronchitis, bronchial asthma, and emphysema. TREATMENT:

4-week treatment with N-acetylcystein administered three times a day 200 mg

dissolved (n = 1734) or undissolved (n = 608) or at some other, usually lower,

dosage (n = 173). During the f-week treatment phase, any other drugs being

taken

were neither discontinued nor changed. TARGET PARAMETERS: In addition to 1-sec

capacity (FEV1), various, mainly subjective, parameters were noted, in

particular coughing, amount and nature of expectorate. RESULTS: for the

evaluation, the patients were assigned either to the acute bronchitis or the

chronic bronchitis group; the latter group also contained patients with other

diseases, such as asthma and emphysema, since such conditions often presented

simultaneously. All selected parameters clearly improved under treatment,

equally in the acute and chronic bronchitis groups. As expected, the mucolytic

effect was very pronounced, the 1-sec capacity increased significantly. No

major

difference was to be found in the results observed in patients on and those not

on other additional medication.

PMID: 1644396 [PubMed - indexed for MEDLINE]

Biochim Biophys Acta 1986 Oct 1;883(3):486-95

Role of directional Ca2+ effect on reduced viscosities of mucus secretions from

chicken trachea in vitro.

Mian N, Kent PW.

Reduced viscosities of fibrillar and gelatinous type mucins produced in

response

to high submucosal Ca2+ and low luminal Ca2+ effects were significantly higher

than those of corresponding types of normal mucins. The increased reduced

viscosity of experimental mucin samples was due to their aggregation with

unique

low molecular weight (mr 325,000 and 46,200) sulphate-rich components. The Ca2+

appeared to exert two opposing effects on viscosity properties of mucins;

whereas Ca2+-dependent complexes between different types of mucins appeared to

be a selective phenomenon between sulphate-rich mucins and components. Ester

sulphate residue content rather than N-acetylneuraminic acid residue content of

these mucins and low molecular weight components showed a very good correlation

with their reduced viscosity and Ca2+-binding values.

PMID: 3092871 [PubMed - indexed for MEDLINE]

[The way I'm reading this is that the sulfated parts of the mucins probably

form a calcium sandwich with the low molecular weight component and that

will make the mucins less viscous, or " globby " .]

Jibiinkoka 1967 Oct;39(10):1117-23 Related Articles, Books, LinkOut

[Non-surgical treatment of chronic sinusitis. Effects of

acetylcysteine into the maxillary sinus]

[Article in Japanese]

Taguchi T, Nishinaga K.

PMID: 5627534 [PubMed - indexed for MEDLINE]

[Guest guest]

Hi ,

I wanted to tell you in my email earlier about why I decided to use Acetyl

cysteine

before I had the answer if it's the same thing with N-acetyl cysteine (other

than

the name, nothing in the prospect indicated that has anything to do with the

sulfur

chemistry), but I thought it may be too much to read and out of the subject. But

now I realize that it might be interesting

I'm not sure why or what this means, but I've noticed that every time I take ALA

I

feel great, absolutely wonderful, better than when I don't take it, but there

was

one small thing: my throat was getting so dry, that it felt almost like an

asthma.

I didn't think much about it, because... many reasons... I usually don't drink a

lot of water (sometimes there are 3-4 days without), I recently had a thyroid

problem, and I thought maybe that's what's causing it... I just didn't bother

much

to find out the explanation for that dry throat.

Lately, the asthma sensation became a really aggravating cough and no matter

what,

in the " on " days I couldn't get rid of it.

So that's what made me see the connection with the mucolityc medicine. So I

tried

it and I only took it 3 times but amazingly, I stopped getting a dry throat when

I

take ALA. It feels great now!

Why did this happen? Why would I need cysteine along with ALA? Can you explain

this

please ? Or tell me what you think... It would help me to understand things

better, because... it seems that me and Denis have the same symptoms to the same

drugs

For example now, with cysteine: we both felt great when we took it (I know I

felt

happier, Denis spoke with people that day), we both had the blister, we both had

the asthma sensation (mine was worse but I heard him breathing while he was

sleeping so I know he had it too).

Do you have any idea why we need cysteine while we already take ALA? Or why

would

ALA require cysteine.

Thank you very much .

Valentina

[Guest guest]

, I read this email with interest as I usually read everything you write.

I want to contribute my 2 cents' worth to it. Even though naprosyn is used by

doctors to treat the pain of arthritis, the world of alternative medicine

believes this product or pain killer actually keeps the cartilage from the

joints from regenerating. This is what happened to me: Because I developed a

frozen arm, the doctor put me on naprosyn to help with the swelling while I did

therapy. I was on naprosyn for about a year as that is how long it took to

unfreeze my arm.. Right after that, I noticed a knocking in my knees. The

doctor said it was osteoarthritis. I subscribed to Dr. Whitaker's Alternatives

Newletter right after that and found out that naprosyn keeps joint cartilage

from regenerating. I have since gotten rid of the osteoarthritis. I took

glucosamine sulfate for a period of time to rebuild my cartilage and eliminate

swelling. Rose

[ ] A segueway into tylenol and medicines for

respiratory infections

,

You asked:

>Does this mean that if I give my hfa son,(6 yrs old), guaifenisen syrup when

>he has respiratory mucus that I want to loosen and have him expel that it

>can cause problems for him by not getting to the lungs?

No, the issue I was presenting is that those with sulfation problems may

end up with TOO much of a dose getting to other organ systems, because an

inappropriately LOW amount of the dose is being disabled in the

gut Prescribed dosages are assuming that a certain amount of the drug

will be processed and disabled in the gut before it ever gets out into the

bloodstream. The dosages are set assuming that process is occurring

normally and will create a blood level within a certain expected range.

I don't know how guafenisen specifically is metabolized, but it is not on

the obvious " bad guy " list as far as demands on the sulfation

chemistry. Some medicines used for sore throats are phenols and say so and

are probably best avoided (like the throat sprays). I know with my

daughter, guafenisen is the cough syrup that seems to work the best.

I'd really like to thank Valentina for mentioning the mucolitic (mucolytic)

properties of NAC, for I chased that yesterday, and found out that NAC has

a long and successful history of being helpful in all sorts of respiratory

situations where there is too much or too " globby " mucus, including

asthma. " Lytic " is a root word that means " breaking something apart " , so

it may be doing the same sort of thing as guafenisin. What a great thing to

find out. I'm really curious about what actually changes, since mucins,

the proteins of mucus, are usually highly sulfated, and sulfated GAGs are

also released from mucus tissues during infection. I wonder if the

mucus becomes less sulfated as it becomes " globbier " ..,you know, that

awful stage when it isn't liquidy any more, and keeps tickling and making

you cough. That stage can last so long after the feeling of being sick is

gone.

Since it seems the sulfate chemistry is sort of put on hold during the main

part of infection, it would seem reasonable to think the end result of

infection might be less sulfate in the mucus...but I'd love to know for sure.

Dr. Waring found out in the laboratory that TNF, an immune factor turned on

during inflammation, suppressed the conversion of cysteine to sulfate in

neurons and GI tract cells. That makes it very interesting to think about

what might be happening with sulfation during this sort of dose of NAC used

for its mucolytic properties. I don't know about mucins particularly, but

with sulfated GAGs, the enzymes that break them apart are looking for a

certain pattern of sulfate to tell the enzyme where to clip the chain in

half. So it may be that adding cysteine at this time helps properly

resulfate these proteins and provide the " key " to breaking up the

" leftovers " .

TPST, the enzyme that sulfates mucins, was measured in autism by Dr.

Waring, and found to be suppressed in activity: in some children almost

completely. One thing that is puzzling about her finding on TNF

suppressing the enzyme that converts cysteine to the first step on the way

to sulfate is that those with AIDS, who of course have horrible problems

with inflammation and too much immune activation, do very well with NAC,

especially in helping to resolve the immune problems that seem to happen as

a result of low sulfur...things like poor natural killer cell activity and

poor T cell cytotoxicity, things that make it hard to keep from getting

sick after an exposure to a disease.

Some children with autism react negatively in a very obvious way to NAC,

but for those who can process it effectively, there is a reason to suspect

it may supply a double benefit during times when there is a respiratory

problem. I had wondered about what it would do for " sinus headaches " , and

was glad to see there was an old unabstracted article about that I've put

below.

Anyway, I've put an example of the NAC/mucolytic articles below. I am very

in favor of finding treatments that WORK, but which don't further strain

the sulfation chemistry.

Pretty much all pain killers strain the sulfate chemistry, but some more

than others. Aspirin and tylenol are BAD in this way. Motrin is sort of

in the middle, and naproxen sodium (naprosyn) seems to put the least strain

on sulfation. I hadn't really heard of naprosyn being used or marketed for

use in children, and wondered why that was, but I did find in the

literature that it is used for children with conditions of chronic pain

like arthritis. So, maybe after the holidays I can make an inquiry with

the manufacturer and get the scoop on whether it is considered safe for

children in other situations. I also know parents whose children, like

mine, don't seem to get any benefit from tylenol anyway. We use motrin,

but only when absolutely necessary and often in half-doses.

I hope this was practical enough for you, . I do the research side,

and am not a doctor, so I'll probably always be more focused on the whys

than the whats, but of course, all of this has to boil down to the " what to

do's " eventually!

Fortschr Med 1992 Jun 30;110(18):346-50

[Therapy of respiratory tract diseases with N-acetylcysteine. An open

therapeutic observation study of 2,512 patients]

[Article in German]

Volkl KP, Schneider B.

Institut fur Biometrie der Med. Hochschule Hannover.

STUDY DESIGN: Open therapeutic observational study. PATIENTS: 2,510 patients

with acute and chronic bronchitis, bronchial asthma, and emphysema. TREATMENT:

4-week treatment with N-acetylcystein administered three times a day 200 mg

dissolved (n = 1734) or undissolved (n = 608) or at some other, usually lower,

dosage (n = 173). During the f-week treatment phase, any other drugs being

taken

were neither discontinued nor changed. TARGET PARAMETERS: In addition to 1-sec

capacity (FEV1), various, mainly subjective, parameters were noted, in

particular coughing, amount and nature of expectorate. RESULTS: for the

evaluation, the patients were assigned either to the acute bronchitis or the

chronic bronchitis group; the latter group also contained patients with other

diseases, such as asthma and emphysema, since such conditions often presented

simultaneously. All selected parameters clearly improved under treatment,

equally in the acute and chronic bronchitis groups. As expected, the mucolytic

effect was very pronounced, the 1-sec capacity increased significantly. No

major

difference was to be found in the results observed in patients on and those

not

on other additional medication.

PMID: 1644396 [PubMed - indexed for MEDLINE]

Biochim Biophys Acta 1986 Oct 1;883(3):486-95

Role of directional Ca2+ effect on reduced viscosities of mucus secretions

from

chicken trachea in vitro.

Mian N, Kent PW.

Reduced viscosities of fibrillar and gelatinous type mucins produced in

response

to high submucosal Ca2+ and low luminal Ca2+ effects were significantly higher

than those of corresponding types of normal mucins. The increased reduced

viscosity of experimental mucin samples was due to their aggregation with

unique

low molecular weight (mr 325,000 and 46,200) sulphate-rich components. The

Ca2+

appeared to exert two opposing effects on viscosity properties of mucins;

whereas Ca2+-dependent complexes between different types of mucins appeared to

be a selective phenomenon between sulphate-rich mucins and components. Ester

sulphate residue content rather than N-acetylneuraminic acid residue content

of

these mucins and low molecular weight components showed a very good

correlation

with their reduced viscosity and Ca2+-binding values.

PMID: 3092871 [PubMed - indexed for MEDLINE]

[The way I'm reading this is that the sulfated parts of the mucins probably

form a calcium sandwich with the low molecular weight component and that

will make the mucins less viscous, or " globby " .]

Jibiinkoka 1967 Oct;39(10):1117-23 Related Articles, Books, LinkOut

[Non-surgical treatment of chronic sinusitis. Effects of

acetylcysteine into the maxillary sinus]

[Article in Japanese]

Taguchi T, Nishinaga K.

PMID: 5627534 [PubMed - indexed for MEDLINE]

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

[Guest guest]

Is glucosamine sulfate used for anything else??? My doctor suggested we use it

and we were talking about so much, I dont know why he recommended it. Any ideas

out there as to what it is for??

[ ] A segueway into tylenol and medicines for

respiratory infections

,

You asked:

>Does this mean that if I give my hfa son,(6 yrs old), guaifenisen syrup

when

>he has respiratory mucus that I want to loosen and have him expel that it

>can cause problems for him by not getting to the lungs?

No, the issue I was presenting is that those with sulfation problems may

end up with TOO much of a dose getting to other organ systems, because an

inappropriately LOW amount of the dose is being disabled in the

gut Prescribed dosages are assuming that a certain amount of the drug

will be processed and disabled in the gut before it ever gets out into the

bloodstream. The dosages are set assuming that process is occurring

normally and will create a blood level within a certain expected range.

I don't know how guafenisen specifically is metabolized, but it is not on

the obvious " bad guy " list as far as demands on the sulfation

chemistry. Some medicines used for sore throats are phenols and say so and

are probably best avoided (like the throat sprays). I know with my

daughter, guafenisen is the cough syrup that seems to work the best.

I'd really like to thank Valentina for mentioning the mucolitic (mucolytic)

properties of NAC, for I chased that yesterday, and found out that NAC has

a long and successful history of being helpful in all sorts of respiratory

situations where there is too much or too " globby " mucus, including

asthma. " Lytic " is a root word that means " breaking something apart " , so

it may be doing the same sort of thing as guafenisin. What a great thing to

find out. I'm really curious about what actually changes, since mucins,

the proteins of mucus, are usually highly sulfated, and sulfated GAGs are

also released from mucus tissues during infection. I wonder if the

mucus becomes less sulfated as it becomes " globbier " ..,you know, that

awful stage when it isn't liquidy any more, and keeps tickling and making

you cough. That stage can last so long after the feeling of being sick is

gone.

Since it seems the sulfate chemistry is sort of put on hold during the main

part of infection, it would seem reasonable to think the end result of

infection might be less sulfate in the mucus...but I'd love to know for

sure.

Dr. Waring found out in the laboratory that TNF, an immune factor turned on

during inflammation, suppressed the conversion of cysteine to sulfate in

neurons and GI tract cells. That makes it very interesting to think about

what might be happening with sulfation during this sort of dose of NAC used

for its mucolytic properties. I don't know about mucins particularly, but

with sulfated GAGs, the enzymes that break them apart are looking for a

certain pattern of sulfate to tell the enzyme where to clip the chain in

half. So it may be that adding cysteine at this time helps properly

resulfate these proteins and provide the " key " to breaking up the

" leftovers " .

TPST, the enzyme that sulfates mucins, was measured in autism by Dr.

Waring, and found to be suppressed in activity: in some children almost

completely. One thing that is puzzling about her finding on TNF

suppressing the enzyme that converts cysteine to the first step on the way

to sulfate is that those with AIDS, who of course have horrible problems

with inflammation and too much immune activation, do very well with NAC,

especially in helping to resolve the immune problems that seem to happen as

a result of low sulfur...things like poor natural killer cell activity and

poor T cell cytotoxicity, things that make it hard to keep from getting

sick after an exposure to a disease.

Some children with autism react negatively in a very obvious way to NAC,

but for those who can process it effectively, there is a reason to suspect

it may supply a double benefit during times when there is a respiratory

problem. I had wondered about what it would do for " sinus headaches " , and

was glad to see there was an old unabstracted article about that I've put

below.

Anyway, I've put an example of the NAC/mucolytic articles below. I am very

in favor of finding treatments that WORK, but which don't further strain

the sulfation chemistry.

Pretty much all pain killers strain the sulfate chemistry, but some more

than others. Aspirin and tylenol are BAD in this way. Motrin is sort of

in the middle, and naproxen sodium (naprosyn) seems to put the least strain

on sulfation. I hadn't really heard of naprosyn being used or marketed for

use in children, and wondered why that was, but I did find in the

literature that it is used for children with conditions of chronic pain

like arthritis. So, maybe after the holidays I can make an inquiry with

the manufacturer and get the scoop on whether it is considered safe for

children in other situations. I also know parents whose children, like

mine, don't seem to get any benefit from tylenol anyway. We use motrin,

but only when absolutely necessary and often in half-doses.

I hope this was practical enough for you, . I do the research side,

and am not a doctor, so I'll probably always be more focused on the whys

than the whats, but of course, all of this has to boil down to the " what to

do's " eventually!

Fortschr Med 1992 Jun 30;110(18):346-50

[Therapy of respiratory tract diseases with N-acetylcysteine. An open

therapeutic observation study of 2,512 patients]

[Article in German]

Volkl KP, Schneider B.

Institut fur Biometrie der Med. Hochschule Hannover.

STUDY DESIGN: Open therapeutic observational study. PATIENTS: 2,510 patients

with acute and chronic bronchitis, bronchial asthma, and emphysema.

TREATMENT:

4-week treatment with N-acetylcystein administered three times a day 200 mg

dissolved (n = 1734) or undissolved (n = 608) or at some other, usually

lower,

dosage (n = 173). During the f-week treatment phase, any other drugs being

taken

were neither discontinued nor changed. TARGET PARAMETERS: In addition to

1-sec

capacity (FEV1), various, mainly subjective, parameters were noted, in

particular coughing, amount and nature of expectorate. RESULTS: for the

evaluation, the patients were assigned either to the acute bronchitis or the

chronic bronchitis group; the latter group also contained patients with

other

diseases, such as asthma and emphysema, since such conditions often

presented

simultaneously. All selected parameters clearly improved under treatment,

equally in the acute and chronic bronchitis groups. As expected, the

mucolytic

effect was very pronounced, the 1-sec capacity increased significantly. No

major

difference was to be found in the results observed in patients on and those

not

on other additional medication.

PMID: 1644396 [PubMed - indexed for MEDLINE]

Biochim Biophys Acta 1986 Oct 1;883(3):486-95

Role of directional Ca2+ effect on reduced viscosities of mucus secretions

from

chicken trachea in vitro.

Mian N, Kent PW.

Reduced viscosities of fibrillar and gelatinous type mucins produced in

response

to high submucosal Ca2+ and low luminal Ca2+ effects were significantly

higher

than those of corresponding types of normal mucins. The increased reduced

viscosity of experimental mucin samples was due to their aggregation with

unique

low molecular weight (mr 325,000 and 46,200) sulphate-rich components. The

Ca2+

appeared to exert two opposing effects on viscosity properties of mucins;

whereas Ca2+-dependent complexes between different types of mucins appeared

to

be a selective phenomenon between sulphate-rich mucins and components. Ester

sulphate residue content rather than N-acetylneuraminic acid residue content

of

these mucins and low molecular weight components showed a very good

correlation

with their reduced viscosity and Ca2+-binding values.

PMID: 3092871 [PubMed - indexed for MEDLINE]

[The way I'm reading this is that the sulfated parts of the mucins probably

form a calcium sandwich with the low molecular weight component and that

will make the mucins less viscous, or " globby " .]

Jibiinkoka 1967 Oct;39(10):1117-23 Related Articles, Books, LinkOut

[Non-surgical treatment of chronic sinusitis. Effects of

acetylcysteine into the maxillary sinus]

[Article in Japanese]

Taguchi T, Nishinaga K.

PMID: 5627534 [PubMed - indexed for MEDLINE]

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

[Guest guest]

Rose,

I am VERY much in agreement with you that it is better to avoid the pain

relievers altogether if you can, and instead do what you can to eliminate

the source of pain, which often enough in adults at least, involves a

problem that may come from impaired sulfation where glucosamine sulfate

will help. There have been trials comparing the two approaches, and the

choice you have made wins hands down in that sort of competition,

especially longterm.

However, I find that a lot of parents agonize over the pain their little

ones experience and WILL choose something to give them for immediate relief

of pain...I think naprosyn may be the least offensive of the pain-killers

to this chemistry, but it is better to treat in different ways when you

can...That is why my chief approach to fever is to let it do its job if it

isn't too high because fever does help kill an invader, but if the

temperature gets too high, use water to cool the skin, whether in the bath

or with a washcloth. This works faster to lower the temperature anyway,

and the pain of fever probably is coming from the effect of changed

temperature on the function of enzymes. So if you get the temp down with

water, you may eliminate the pain as well as the temperature.

The advice that really makes me cringe is to give a child tylenol

prophylactically for pain due to vaccination. That is a good formula for

depressing the immune system at a very critcal time, and to make the gut

more vulnerable to infections itself, and it may even change the ability

for the immune system to make more precise antibodies. The body needs all

the sulfur it can muster to keep lymphocytes properly cytotoxic. I really

suspect that giving a child tylenol during infection may make it much

harder for the immune system to respond properly. It is a great folly that

we've been taught to " pop a tylenol " at the least provocation.

Good for you in fnding an approach that really worked.

J Immunol 1986 Oct 15;137(8):2522-7 Related Articles, Books, LinkOut

IgG subclasses of anti-tetanus toxoid antibodies in adult and newborn

normal subjects and in patients with systemic lupus erythematosus,

Sjogren's syndrome, and drug-induced autoimmunity.

Rubin RL, Tang FL, Lucas AH, Spiegelberg HL, Tan EM.

The IgG subclasses of anti-tetanus toxoid (anti-TT) antibodies were

quantitated in normal sera and sera from patients with rheumatic disease.

Detection relied on a set of four mouse monoclonal antibodies, each of

which showed specificity for the respective isotype, independent of

gamma-chain allotype or light chain class of the human antibody.

Approximately 90% of the total anti-TT activity in normal adults and

patients with Sjogren's syndrome was IgG1. In addition, IgG4 antibodies

were detected in one-half the samples, but IgG2 and IgG3 antibodies were

observed in only two out of 36 sera. However, antibodies elicited in

children immunized with TT were exclusively IgG1 and IgG3, with IgG4

antibodies detectable only at birth (presumably due to transplacental

passage of antibody) in three of 12 children. In contrast to normal adults,

patients with systemic lupus erythematosus (SLE) and drug-induced

autoimmunity (DIA) had a more promiscuous isotype profile. IgG2 and/or IgG3

anti-TT antibodies were detected in 13 of 22 SLE patients and IgG3

antibodies in six of 11 patients with DIA. IgG4 anti-TT antibodies were

predominant in seven of these 33 patients. These findings suggest that IgG

isotypes may depend on the frequency of the stimulus, but global

alterations in immunologic status as reflected in systemic autoimmune

disease may override the homeostatic mechanisms that control isotype

restriction.

PMID: 3760565 [PubMed - indexed for MEDLINE]

At 06:04 PM 2/23/2002 -0600, you wrote:

>, I read this email with interest as I usually read everything you

>write. I want to contribute my 2 cents' worth to it. Even though

>naprosyn is used by doctors to treat the pain of arthritis, the world of

>alternative medicine believes this product or pain killer actually keeps

>the cartilage from the joints from regenerating. This is what happened to

>me: Because I developed a frozen arm, the doctor put me on naprosyn to

>help with the swelling while I did therapy. I was on naprosyn for about

>a year as that is how long it took to unfreeze my arm.. Right after that,

>I noticed a knocking in my knees. The doctor said it was

>osteoarthritis. I subscribed to Dr. Whitaker's Alternatives Newletter

>right after that and found out that naprosyn keeps joint cartilage from

>regenerating. I have since gotten rid of the osteoarthritis. I took

>glucosamine sulfate for a period of time to rebuild my cartilage and

>eliminate swelling. Rose

>

> Pretty much all pain killers strain the sulfate chemistry, but some more

> than others. Aspirin and tylenol are BAD in this way. Motrin is sort of

> in the middle, and naproxen sodium (naprosyn) seems to put the least

> strain

> on sulfation. I hadn't really heard of naprosyn being used or marketed

> for

> use in children, and wondered why that was, but I did find in the

> literature that it is used for children with conditions of chronic pain

> like arthritis.

[Guest guest]

> Is glucosamine sulfate used for anything else??? My doctor suggested we use

it and we were talking about so much, I dont know why he recommended it. Any

ideas out there as to what it is for??

Hi ,

Glucosamine sulfate is a great supplement I'm in love with it, but... I also

have a problem that interferes with the way glucosamine sulfate works in my body

and I have to stay away from it. Too bad.

Glucosamine sulfate (as Rose said) is usually great for joints to treat

arthritis or rheumatism or other similar stuff.... (I don't really know a lot

about this)

It is very important in the sulfur chemistry. It supplies sulfate for the PST

activity. It stimulates the synthesis of the GAGs and it has an

anti-inflammatory action. It helps the cells to resist infection and it has a

powerful effect against lipid envelope viruses (at least that's what I've read

about it)

My problem was with the fact that I have high ammonia. Glucosamine supplies

glutamine, which is great for the intestines but not when you have high ammonia.

(I am not sure if I could still take Glucosamine and Alpha Ketoglutaric Acid in

the same time...)

Anyway, hope this helps...

Valentina

[Guest guest]

Here are some more uses: helps osteoarthritis by providing the

sulphate to make cartilage; helps tendinitis; used in muscle injury

prevention; helps strengthen tendons and ligaments; helps

inflammation and provides some pain relief in osteoarthritis; and

lately, I believe, I have heard it is also used for the pain and

inflammation of rheumatoid arthritis. Rose

-- In @y..., Valentina Ardelean <val@t...> wrote:

> > Is glucosamine sulfate used for anything else??? My doctor

suggested we use it and we were talking about so much, I dont know

why he recommended it. Any ideas out there as to what it is for??

>

> Hi ,

>

> Glucosamine sulfate is a great supplement I'm in love with it,

but... I also have a problem that interferes with the way glucosamine

sulfate works in my body and I have to stay away from it. Too bad.

> Glucosamine sulfate (as Rose said) is usually great for joints to

treat arthritis or rheumatism or other similar stuff.... (I don't

really know a lot about this)

>

> It is very important in the sulfur chemistry. It supplies sulfate

for the PST activity. It stimulates the synthesis of the GAGs and it

has an anti-inflammatory action. It helps the cells to resist

infection and it has a powerful effect against lipid envelope viruses

(at least that's what I've read about it)

>

> My problem was with the fact that I have high ammonia. Glucosamine

supplies glutamine, which is great for the intestines but not when

you have high ammonia.

> (I am not sure if I could still take Glucosamine and Alpha

Ketoglutaric Acid in the same time...)

> Anyway, hope this helps...

>

>

> Valentina

[Guest guest]

Could you please tell me how you test for ammonia? Thanks.

[ ] Re: A segueway into tylenol and medicines for

respiratory infections

> > Is glucosamine sulfate used for anything else??? My doctor suggested we

use it and we were talking about so much, I dont know why he recommended it.

Any ideas out there as to what it is for??

>

> Hi ,

>

> Glucosamine sulfate is a great supplement I'm in love with it, but... I

also have a problem that interferes with the way glucosamine sulfate works

in my body and I have to stay away from it. Too bad.

> Glucosamine sulfate (as Rose said) is usually great for joints to treat

arthritis or rheumatism or other similar stuff.... (I don't really know a

lot about this)

>

> It is very important in the sulfur chemistry. It supplies sulfate for the

PST activity. It stimulates the synthesis of the GAGs and it has an

anti-inflammatory action. It helps the cells to resist infection and it has

a powerful effect against lipid envelope viruses (at least that's what I've

read about it)

>

> My problem was with the fact that I have high ammonia. Glucosamine

supplies glutamine, which is great for the intestines but not when you have

high ammonia.

> (I am not sure if I could still take Glucosamine and Alpha Ketoglutaric

Acid in the same time...)

> Anyway, hope this helps...

>

>

> Valentina

>

>

>

>

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

>