Asthma

[Guest guest]

[This message contained attachments]

[Guest guest]

Hi Larry, I don't recall reading anything about Lyme and Asthma. But what I

found unusual with my son is that he has had Infection triggered asthma since

he was very young, but did not have his full blown asthma with lyme. He felt

winded a lot with exercize and constant nasal congestion, but no coughing and

wheezing. I can't figure it out.

[Guest guest]

Hi,

My asthma get steadily worse since lyme. It drives me nuts. Everyone around

here got sick this spring. I swear there was bacteria in the pollen.

connie, MI

[Guest guest]

--- Cslyme@... wrote:

> From: Cslyme@...

>

> Hi,

> My asthma get steadily worse since lyme. It drives

> me nuts. Everyone around

> here got sick this spring. I swear there was

> bacteria in the pollen.

> connie, MI

>

> Connie-

Not to mention our wonderful water.

L

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[Guest guest]

Hi L

LOL about our water,

Connie, MI

[Guest guest]

--- Cslyme@... wrote:

> From: Cslyme@...

>

> Hi L

> LOL about our water,

> Connie, MI

>

> Connie-

That has always been my excuse for not drinking it. Figured it would do

more harm than good. But now I have a warter filter so guess I dont

have that excuse anymore.

L

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[Guest guest]

My asthma has gotten worse as the lyme lingers on. But this year my doctor

said that all his patient have gotten infections after an asthma/allergy

attack. I asked him if there was bacteria in the pollen this year. He said,

maybe, that's a thought,

Connie, MI

[Guest guest]

Marta,

Here is Dr. Edell's web address. You can subscribe from here.

http://www.healthcentral.com/

Larry

[Guest guest]

Thanks Larry,

I will check it out. I heard on last night's Nightly News with Tom Brokaw,

that C. Everett Koop's new website, is earning him $44 million dollars! Not

bad, just for lending his name. Unfortunately the information he is providing

about Lyme disease is really bad, old stuff from Steere/Sigal. I also heard the

stock for his website doubled in one day! Wish I had some of it. I like Dr

Edell, and hope he is making decent money from his site, I trust him for some

reason.

Feel good,

Marta

Re: [Lyme-aid] Asthma

ÿþ

Marta,

Here is Dr. Edell's web address. You can subscribe from here.

http://www.healthcentral.com/

Larry

[Guest guest]

To all,

I found this to be an interesting article, well documented, though it's

fairly old.

Larry

LYME DISEASE: THE SENSIBLE PURSUIT OF ANSWERS

B. Liegner

Lyme Borreliosis and Related Disorders, Internal and Critical Care Medicine

8 Barnard Road, Armonk, New York 10504

Journal of Clinical Microbiology, Aug. 1993, p. 1961-1963

" Disease is very old and nothing about it has changed. It is we who

change as we learn to recognize what was formerly imperceptible. "

_ Charcot, De l'Expectation en Medecine

In 1989, Preac-Mursic et al. published a landmark article (30) documenting

recovery by culture of living Borrelia burgdorferi from patients who had been

previously treated with regimens believed to cure the disease. Included was one

patient who had been treated with 10 days of intravenous ceftriaxone and from

whose spinal fluid the organism was grown following treatment (30) This report

was greeted with skepticism and disbelief from some quarters, with suggestions

the cultures must have been contaminated or that the report was otherwise

erroneous. Since then there have been a number of corroborating reports

confirming survival of B. burgdorferi in humans despite aggressive antibiotic

treatment, including the use of the best available intravenous antibiotics (12,

22). These apparently anomalous observations, which reveal the deficiencies of

the existing paradigm for Lyme disease, have been very hard for the medical

community to reconcile, and they presage a revolution in our conceptualization

of this disease (15). Such a shift will be necessary to deal effectively with

the biologic realities of B. burgdorferi infection (1).

Emerging scientific research is beginning to clarify how it is possible for a

bacterial infection to resist eradication by the powerful antibiotics employed

against it. Montgomery et al. reported on the intracellular localization of B.

burgdorferi within macrophages and the recovery of spirochetes in culture from

these cells (29). Klempner, Georgilis, and coworkers demonstrated very

convincingly that B. burgdorferi can adopt an intracellular location within

fibroblasts and that the organism can be grown from such cells in vitro after

treatment of the tissue cultures with ceftriaxone (9, 14). Ma et al. reported on

the intracellular localization of B. burgdorferi within human umbilical vein

endothelial cells in vitro (25). In a recent editorial, Mahmoud points out that

infections due to intracellular pathogens are notoriously difficult to treat and

cure (26). Interestingly, B. burgdorferi was not among the list of pathogens

cited. The author suggested that the outcome of infections due to intracellular

pathogens may be genetically regulated. Steere et al. have suggested that

genetic regulation may be a feature of infections due to B.burgorferi; they

found the illness more problematic in individuals bearing HLA-DR 2, 3, or 4

alleles (33). The key to the development of methods to combat such infections,

Mahmoud argues, is increased understanding of adhesion to and internalization in

host cells by these pathogens. Monco et al. (8), Coburn et al. (1a), and

others are intensively studying this process in B. burgdorferi infection.

These observations lead one to the conclusion that certain subsets of patients

with Lyme disease may require prolonged antibiotic treatment and that presently

available chemotherapeutic modalities may be suppressing but not eradicating the

infection. Thus, individuals who have demonstrated relapses following aggressive

treatment may require an open-ended antibiotic approach provided that they are

deriving clinical benefit and not experiencing any adverse effects and that they

wish to be treated (24). Oral antibiotics often suffice to keep patients well,

and these are certainly preferable in terms of convenience and cost. It should

be emphasized, however that all oral regimens should be designed to adequately

treat not only the musculoskeletal system and other peripheral locations but

also the central nervous system (7, 17, 19). Unfortunately, some patients do not

respond adequately to oral medication, particularly those with serious central

nervous system involvement, and in such individuals, prolonged intravenous

treatment may be necessary. In one such case, B. burgdorferi was grown from

spinal fluid despite treatment for 21 days with parenteral cefotaxime and 4

months with minocycline (22). This patient had virtually no opportunity for

reinfection in the interim. Cerebrospinal fluid pleocytosis which had been

present for several years and which failed to improve with a prior course of 21

continuous days of intravenous cefotaxime resolved completely with 13 weeks of a

" pulse " cefotaxime regimen (11) consisting of 4 g. every 8 h. for 24 h. weekly.

Significant neurologic injury injury had already occured in this patient.

However, because of the known plasticity of the human central nervous system, it

is hoped that suppression of the infectious agent with extended treatment will

at least avoid or slow further microbe-induced damage and that perhaps some

recovery of neurologic function may occur in time.

Many clinicians and scientists admit that seronegative Lyme disease exists but

maintain that it is a rare phenomenon. Indeed, for study purposes, many academic

centers have specifically excluded patients presenting with symptoms possibly

compatible with Lyme disease who are seronegative. This may be a serious

conceptual and methodological error. Present understanding of the human immune

response to B. burgdorferi infection is rudimentary. Antibody response, although

strong and invariable in some individuals, may wax and wane over time.

Diagnostic serologic titers may be undetectable in other patients for reasons

that are presently poorly understood. At least four research groups have

suggested the presence of immune complexes in the sera and/or cerebrospinal

fluid of patients with Lyme disease (3, 5, 10, 32). In patients for which a

state of antigen excess exists, free antibodies may escape detection and may be

revealed only after use of methods to dissociate such immune complexes. Thus,

the very patients who are unable to generate detectable levels of free

antibodies, who are least apt to contain the infection, and who may present with

the more serious illness among those with Lyme disease are least likely to be

offered treatment. For example, the patient described above was seronegative for

the first 5 years of her illness, during which time she sustained severe and

irreversible neurologic injury. Western immunoblot serologic results were

inconclusive at the time B. burgdorferi was isolated from the CSF, highlighting

the fallacy of the use of this test as a " gold standard " for the confirmation of

Lyme disease. An antigen-capture assay developed by the Rocky Mountain

Laboratory of the National Institute for Allergy and Infectious Disease (6)

demonstrated shedding of B. burgdorferi-specific antigen in the urine of many

patients who were suspected of having Lyme disease but who were seronegative

with usual antibody tests (21). The availability of such direct antigen

detection methods, the polymerase chain reaction, and other approaches which

directly demonstrate the presence of the pathogen, once clinically validated,

will foster more rational pharmacotherapy for Lyme disease. Results of such

assays will promote recognition of that which astute clinicians have long

inferred from the careful study of their patients, that seronegativity is a real

phenomenon in Lyme disease, occurring in both early and late stages(4, 21).

Acceptance of the possibility of seronegative disease makes empirical treatment

for patients in whom Lyme disease is clinically suspected imperative, even if

serologic tests are negative. Obviously, such commitment to therapy should occur

only after thorough but expeditious efforts have failed to identify another

cause for the symptoms. Early occurrence of irreversible neurologic injury,

although rare (23, 28), may be avoided by prompt and specific therapy for such

patients.

The increasing realization that Lyme disease, once entrenched, may be a chronic

persisting infection refractory to cure with presently available therapeutic

approaches in some patients gives added cogency to the argument in favor of

preventive treatment of deer tick bites, particularly when ticks have been

attached long enough to become engorged. Eradication of the spirochete before

dissemination and adoption of an intracellular location is of great advantage

(16, 18, 20).

Chronic persisting infection not yielding to antibiotic treatment presents a

dilemma for the patient, the physician, and for insurance companies that are

contractually obliged to pay for medically necessary treatment (34). The

solution is not denial of the reality of patient illness or imposition of

arbitrary restrictions on allowable durations of treatment but the design of

more effective and less costly treatments that can keep the patients well. Aside

from prevention of the illness in the first place, methods achieving sure cure

for those already infected must be developed. Antibiotics may not be the answer.

Rather, application of new techniques of molecular biology to interfere

irreversibly with key metabolic or reproductive processes of the bacterium

wherever it may be found in the body, including intracellular sites, may provide

more effective targeted therapy in the future (2, 13, 27, 31, 35).

A major shift in paradigm is underway regarding the nature of Lyme disease and

the treatment of infected patients. Objective markers for disease activity,

presently research tools (4, 6, 21), will permit the true scope of chronic

persisting infection and seronegative disease to be appreciated. This will allow

the effectiveness of various treatment options to be gauged and guide the

development of superior approaches. Lyme disease, complex and mysterious, will

continue to pose difficult problems for us, for our patients, and for our

society as human intelligence strives to fathom and checkmate B. burgdorferi, a

biologic " evil genius " .

REFERENCES

1. Brenner, C. 1992. Lyme disease. Asking the right questions.

Science 257:1845.

1a.Coburn, J., J. Leong, and J. Erban. Unpublished data.

2. Cohen, J. 1993. Naked DNA points the way to vaccines.

Science 259:1691-1692.

3. Coyle, P. K., A. L. Belman, and B. Krupp. 1992. B. burgdorferi-specific

immune complexes in cerebrospinal fluid, abstr. 167, p. A29. Program

Abstr. 5th Conf. Lyme Borreliosis. 1992.

4. Coyle, P.K.. S. E. Schutzer, A.L. Belman, L.B. Krupp, and Z.Dheng.

1992. Cerebrospinal fluid immunologic parameters in neurologic Lyme

disease, p. 31-43. In S. E. Schutzer (ed), Lyme disease molecular and

immunologic approaches. Current communications in cell and molecular

biology . Cold Spring Harbor Laboratory Press, Cold Spring Harbor, N.Y.

5. Dorward, D., E. D. Huhuenel, G. , and C. F. Garen.. 1992.

Extracellular Borrelia burgdorferi proteins interact with

non-borrelia-directed IgM antibodies. abstr. 219, p. A38. Program Abstr.

5th Int. Conf. Lyme Borreliosis, 1992.

6. Dorward, D. W., T. G. Schwan, and C. F. Garon. 1991. Immune capture and

detection of B. burgoferi antigens in urine, blood, or tissues from

infected ticks, mice, dogs, and humans. J. Clin. Microbiol. 29: 1162-1170.

7. Faber, W. R.., J. D. Bos, P. J. G. M. Rietra, H. Fas, and R. V. W. Van

Eijk. 1983. Treponemicidal levels of amoxicillin in cerebrospinal fluid

after oral administration. Sex. Transm. Dis. 10:148-150.

8. Monco, J. C., B. Fernandez Villar, and J. L. Benach. 1989.

Adherence of Lyme disease spirochetes to glial cells and cells of glial

origin. J. Infect. Dis. 160:497.

9. Georgilis, K., M. Peacocke, and M. S. Klempner. 1992 Protection of the

Lyme disease spirochete, B. burgdorferi from ceftriaxone by human skin

fibroblasts, abstr. 165. p. A29. Program Abstr. 5th Int. Conf. Lyme

Borreliosis. 1992.

10.Hardin, J. A., A. C. Steere, and S. E. Malawista. 1979. Immune

complexes and the evolution of Lyme arthritis. Dissemination and

localization of abnormal C1q binding activity. N. Engl. J. Med.

301:1358-1363.

11. Hassler, D., K, Riedel, J. Zorn, and V. Preac-Mursic. 1991. Pulsed

high-dose cefotaxime therapy in refractory Lyme borreliosis. Lancet

338:193.

12. Haupi, T.. A. Krause, M. Rittig, C. Schoerner, J. R. Kalden, M. Simon,

R. Wallich, and G. R. Burmester. 1992. Persistence of B. burgdorferi in

chronic Lyme disease: altered immune regulation or evasion into

immunologically privileged sites?. abstr. 149, p. A26. Program Abstr. 5th

Int. Conf. Lyme Borreliosis. 1992.

13. Holden, C. 1992. Random samples: another gene therapy first. Science

256:1628.

14. Klempner, M. S., R. Noring, M. Peacocke, K. Georgilis, C. Braden, and

R. A. . 1992. Invasion of human skin fibroblasts by the Lyme

disease spirochete, B. burgdorferi. abstr. 164, p. A29. Program Abstr, 5th

Int. Conf. Lyme Borreliosis, 1992.

15. Kuhn, T. S. 1963. The structure of scientific revolutions. University

of Chicago Press, Chicago.

16. Liegner, K. B. 1990. Lyme disease. N. Engl. J. Med. 322:474-475.

17. Liegner, K. B. 1992. Minocycline in Lyme disease. J. Am. Acad.

Dermatol. 26:263-264.

18. Liegner, K. B. 1993. Prevention of Lyme disease after tick bites. N.

Engl. J. Med. 328:136-137.

19. Liegner, K. B. 1993. Minocycline in Lyme disease. J. Am.Acad.

Dermatol. 28:131.

20. Liegner, K. B. A controlled trial of antimicrobial prophylaxis for

Lyme disease after deer-tick bites. N. Engl. J. Med. in press.

21. Liegner, K. B., D. Dorward, and C. Garon. 1992. Lyme borreliosis (LB)

studied with the Rocky Mountain Laboratory (RML) antigen-capture assay in

urine. abstr. 104, p. A18. Program Abstr. 5th Int. Conf. Lyme

Borreliosis,1992.

22. Liegner, K. B., C. E. Rosenkilde, G. L. , T. J. Quan, and D.

T. Dennis. 1992. Culture-confirmed treatment failure of cefotaxime and

minocycline in a case of Lyme meningoencephalomyelitis in the United

States, abstr. 63, p. A10. Program Abstr. 5th Int. Conf. Lyme

Borreliosis,1992.

23. Liegner, K. B., and J. Selman. 1992. Global cerebellar atrophy in Lyme

borreliosis. abstr. 55B, p. A10. Program Abstr. 5th Int. Conf. Lyme

Borreliosis, 1992.

24. Liegner, K. B., J. R. Shapiro, D. Ramsay, A. J. Halperin, W. Hogrefe,

and L. Kong. 1993. Recurrent erythema migrans despite extended antibiotic

treatment with minocycline in a patient with persisting B. burgdorferi

infection. J. Am. Acad. Dermatol. 28:312-314.

25. Ma, Y., A. Sturrock, and J. Weis. 1991. Intracellular localization of

B. burgdorferi within endothelial cells. Infect. Immun. 59:671-678.

26. Mahmoud, A. A, F. 1992. The challenge of intracellular pathogens. N.

Engl. J. Med. 326:761-762.

27. Mergny, J. L., G. Duval-Valentin, C. H. Nguyen, L. Perrouault, B.

Faucon, M. Rougee, T. Montenay-Garestier, E. Bisagni, and C. Helene. 1992.

Triple Helix-specific ligands. Science 256:1681-1983.

28. Merlo, A., B. Weder, E. Ketz, and L. Matter. 1989. Locked-in state in

B. burdorferi meningitis. J. Neurol. 236:305-306.

29. Montgomery, R. R., M. H. son, and S. E. Malaista. 1992. The

fate of B. burgdorferi in mouse macrophages: destruction, survival,

recovery, abstr. 143, p. Ast Program Abstr. 5th Int. Conf. Lyme

Borreliosis, 1992.

30. Preac-Mursic, V,, K. Weber, W. Pfister, B Wilske, B. Gross, A. Bauman,

and J. Prokop. 1989. Survival of B. burgdorferi inantibiotically treated

patients with Lyme borreliosis. Infection 17:355.

31. , R. W., and D. M. Crothers. 1992. Stability and properties of

double and triple helices: dramatic effects of RNA or DNA backbone

composition. Science 258:1463-1466.

32. Schutzer, S. E., P. K. Coyle, and M. Brunner. 1992. Specific serum

immune complexes in Lyme disease. abstr. 135, p. A24. Program Abstr. 5th

Int. Conf. Lyme Borreliosis, 1992.

33. Steere, A. C., E. Dwyer, and R. Winchester. 1990. Association of

chronic Lyme arthritis with HLA-DR4 and HLA-DR2 alleles. N. Engl. J. Med.

323:212-223.

34. Sullivan, P. 1992. Health insures limit drugs for Lyme disease. Sunday

Star Ledger. Newark, N. J., volume 79 March 22. Section E. p. 1.

35. Szuromi, P. 1992. Triple-helix preference. Science 256:1607.

[Guest guest]

Thanks Larry,

Dr Leigner is a friend to us, even 6 years later he is still working hard to

try to help us. Excellent article.

Marta

To all,

I found this to be an interesting article, well documented, though it's

fairly old.

Larry

LYME DISEASE: THE SENSIBLE PURSUIT OF ANSWERS

B. Liegner

Lyme Borreliosis and Related Disorders, Internal and Critical Care Medicine

8 Barnard Road, Armonk, New York 10504

Journal of Clinical Microbiology, Aug. 1993, p. 1961-1963

[Guest guest]

To all,

FYI

Larry

http://www.healthcentral.com/news/newsfulltext.cfm?ID=13124

[Guest guest]

In a message dated 6/14/99 8:22:44 AM Eastern Daylight Time,

mimianne@... writes:

<< The

simplest and least expensive would be to change the diet to the one

described on my web site at under the tab Read This First. >>

I'd love to see the site. Can you send a link?

, New Bedford, MA.

<A HREF= " http://members.tripod.com/LymeDizzez/ " >Lyme Disease and Me</A>

ICQ # 26791014

[Guest guest]

john bulanda <jbulanda@...> wrote:

Hello everyone,

I was wondering if anyone else has asthma in addition to their Psoriatic

Arthritis. ,I have a mild form of Asthma...I had it when I was a child, out

grew it and it returned in '85. I'm not bothered with it too much except when

I'm around a cat or during a high pollen count. Mostly cats though. I had a good

attack in May when I was at my mother's. She has a cat...woke up in the middle

of the night gasping for air. Finally got relief after using my inhaler. I am

usually okay. Have you been diagnosed with PA? Sounds like you've had a rough

year. Hang in there..we're all here to listen and to help if we can. Donna

Get Your Private, Free E-mail from MSN Hotmail at http://www.hotmail.com

[Guest guest]

Hi ,

I was just curious as to how long you took vioxx. I have been taking it for

about a month now and boy do i feel the difference if i miss a day or two. I

take 25 mg. per day.

Angie

john bulanda <jbulanda@...> wrote:

The vioxx helped me get

through the worst of the pain and I have been off it now for 3 months.

[Guest guest]

,

I have asthma, PS and Hep C. So there. MTX really makes my asthma worse and

I feel too sick, so it's not an option. I get complete control with

Asthmacort. It doesn't screw you up like prednisone, so they say, 'cause

it's inhaled in very small doses. Some of the new asthma drugs help

infalmation so they help both diseases.

Doing a lot of housekeeping and laundry is harder too, with arthritis, and

many of people have dust mite allergies so they should wash their bedding

frequently, dust and vacuum.

bana

________________________________________________________________________

Get Your Private, Free E-mail from MSN Hotmail at http://www.hotmail.com

[Guest guest]

> 5 yo son occasionally has wheezing episodes during/after colds, for

which we

> have to use the nebulizer or at least the spacer with albuterol. The

drug

> makes him feel wretched and he's impossible -- slapping his sister

in the face,

> totally irrational and furious. Has anyone found any alternatives to

albuterol?

Do you use cold medication? In my family, asthma is caused by milk

and artificial colors, and enzymes only help a little.

Dana

[Guest guest]

My son did poorly on Albuterol (po and nebs) but does fine on nebulized

Xopenex.

Kathy

Re: asthma

>

> > 5 yo son occasionally has wheezing episodes during/after colds, for

> which we

> > have to use the nebulizer or at least the spacer with albuterol. The

> drug

> > makes him feel wretched and he's impossible -- slapping his sister

> in the face,

> > totally irrational and furious. Has anyone found any alternatives to

> albuterol?

>

>

> Do you use cold medication? In my family, asthma is caused by milk

> and artificial colors, and enzymes only help a little.

>

> Dana

>

>

>

>

>

>

>

[Guest guest]

Hi,

You may want to try looking at the website called Asthmaworld--it is a site

by researchers in Canada who have used supplements successfully. MILK is a big

issue for my NT son. Something like 40% of kids have allergies to milk

proteins. Once we eliminated the milk, the asthma stopped. The supplements

suggested in AsthmaWorld helped a bunch, too. I have heard the same thing from

several friends now. They got rid of the asthma by the elimination of milk and

the

adding of a few supplements.

in Salt Lake CIty

[Guest guest]

I have read that glutathione helps some kids with asthma.. increasing

omega 3's...

I know the med makes them feel all icky but the consequence of not

using albuterol is worse. If he needs it, you have to use it

otherwise the lungs get more damage with each asthma attack. I

wonder if an epsom salt bath after the albuterol would help him calm

down??

And I don't really want to plug that tea again, BUT, the herbs in

ojibwa tea of life do help lung function, according to the literature

that comes with it. ;-)

My son has asthma too and we started a traditional chinese medicine

practice of having certain herbs applied to acupoints on his upper

back-- will have to do it twice a year for three years in a row. We

just did the first application a month ago... so far so good. The

fall/winter season will tell us if there was any improvement or not,

since that's when Ethan gets upper respiratory issues.

W

> 5 yo son occasionally has wheezing episodes during/after colds, for

which we

> have to use the nebulizer or at least the spacer with albuterol.

The drug

> makes him feel wretched and he's impossible

[Guest guest]

In a message dated 7/30/03 10:19:59 AM, danaatty@... writes:

<< Do you use cold medication? >>

I haven't found anything for kids that's not full of dyes and/or aspartame.

Do you know of any that's good?

Nell

[Guest guest]

In a message dated 7/30/03 4:31:36 PM, maryandphilip@... writes:

<< My son has asthma too and we started a traditional chinese medicine

practice of having certain herbs applied to acupoints on his upper

back-- will have to do it twice a year for three years in a row. We

just did the first application a month ago... so far so good. >>

Good luck, , and report back! My son gets an Epsom bath every night; it

doesn't seem to help the nasty albuterol reaction so at this point I'm just

resigned to waiting it out. He's gone pretty long stretches (9 months, 6 months)

with no asthma episodes but lately he's had several. Yet another

mystery...he's already taking EFAs and I'm starting him on Ojibwa tea tonight!

Nell

[Guest guest]

>

> In a message dated 7/30/03 10:19:59 AM, danaatty@y... writes:

>

> << Do you use cold medication? >>

>

> I haven't found anything for kids that's not full of dyes and/or

aspartame.

> Do you know of any that's good?

For my kids, I don't use children's cold medicine. I use adult

caplets and chop them up. The adult medicines [which are caplets and

not liquid] have fewer artificials.

Dana

[Guest guest]

In a message dated 8/3/03 3:12:55 AM, dhooten@... writes:

<< Many times filling the nebulizier with just the saline does the trick for

my son.

>>

Great idea! Where do you get the saline? Do you make it yourself?

Nell

[Guest guest]

Many times filling the nebulizier with just the saline does the trick for

my son.

jennifer

asthma

> 5 yo son occasionally has wheezing episodes during/after colds, for which

we

> have to use the nebulizer or at least the spacer with albuterol. The drug

> makes him feel wretched and he's impossible -- slapping his sister in the

face,

> totally irrational and furious. Has anyone found any alternatives to

albuterol?

> The instant the cold hit I gave him a little olive leaf extract but it

made

> his stomach hurt. Being on Feingold has lessened these episodes

considerably,

> but UGH I hate this breathing stuff.

>

> Nell

>

>

>

>

>