NAC and candida; thiamine deficiency

[Guest guest]

Listmates,

I've heard some concern that taking sulfur supplements may enhance the

multiplication of candida.

My daughter is now over the flu, and right on schedule, her immune system

seems to have shifted (probably to TH2) and she is having a yeast infection.

Since I've been giving her N-acetyl-cysteine for some time without any

problem, I thought it would be good to look in the literature and see if

there was a track record for using NAC when candidiasis was an issue, and

there was. In vitro, it significantly helped the antifungal activity of

peripheral blood monocytes.., ie NAC helped to kill candida by enhancing

the killing power of monocytes. The study didn't see this positive effect

in vivo in patients with chronic obstructive pulmonary disease, where

candidiasis is apparently a big problem, but it may be because the NAC was

utilized before it got to the lungs, especially if there were sulfur

problems elsewhere. It is good to know that there was NO MENTION of this

form of cysteine causing candida to take off growing. Since my daughter

has had an immune evaluation that found low cytotoxicity in two types of

blood cells, I think continuing with the NAC for her is a very good idea.

I have wondered if the children who were having problems with NAC or other

sulfur supplements were children with symptoms or altered lab values that

are seen in thiamine deficiency, so I would like to bring a little

attention to thiamine. This vitamin (B1) also contains sulfur and is made

from cysteine, and it may be important to assess and address its deficiency

before enhancing other parts of the downstream sulfur pathway.

For a description of thiamine deficiency, please see the online Merck manual:

http://www.merck.com/pubs/mmanual/section1/chapter3/3j.htm

I found this interesting at that site : there is some sort of thiamine

resistence that is associated with low blood magnesium and corrected with

mag. sulfate, ie., the same thing as epsom salts.

" Magnesium, a cofactor for transketolase, should be given as magnesium

sulfate (1 to 2 mL IM of a 50% solution) with thiamine to correct thiamine

resistance and the frequently accompanying hypomagnesemia. "

It would be wonderful to find an explanation for the low magnesium levels

that are seen sometimes in autism.

Another site:

http://kobiljak.msu.edu/CAI/Pathology/Toxic_F/Toxic_4b.html

from Michigan State University spoke about its interaction with ALA:

Thiamine is a coenzyme for the decarboxylation of pyruvate and the

oxidation of alpha keto-glutamic acid. Lipoic acid which is formed in the

liver is also required for the reactions. Patients with liver disease may

show signs of B1 deficiency, possibly because of deficient synthesis of

lipoic acid. In vitro, thiamine deficiency produces accumulation of

pyruvate and lactate, reduction of acetate, citrate and

alpha-keto-glutarate and reduced acetylcholine synthesis. Any of these

metabolic changes could be involved in dysfunction.

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

I know I've seen some labs with children with low citrate, so I will try to

go and review those again and see if I see those other markers. It may be

that some of the children seeing benefits from ALA during chelation may be

seeing an improvement in thiamine issues.

Wernicke's encephalopathy is known to be associated with thiamine

deficiency, and it can present in different ways, and not usually with the

accepted " triad " that is definitional for the syndrome: nystagmus, ataxia

and confusion. That the symptoms are reminiscent of problems seen in

autism is suggested by an article below, stating just that suspicion.

For a very nice discussion of this form of thiamine deficiency, see:

http://www.bcm.tmc.edu/neurol/challeng/pat54/summary.html

At any rate, I'm sure many of us would be delighted to hear from any

listmates who look at these or other thiamine deficiency sites and find any

odd symptoms or laboratory findings there that have been an issue in your

children or yourself.

Some of the symptoms listed at these sites seemed a lot like B12

deficiency, which my father had in the form of pernicious anemia. Now, I

wonder about the thiamine side, as that was certainly not evaluated, but

there is literature suggesting it should have been!

Chest 1994 Mar;105(3):806-11 Related Articles, Books, LinkOut

Macrophage activation by N-acetyl-cysteine in COPD patients.

Vecchiarelli A, Dottorini M, Pietrella D, Cociani C, Eslami A, Todisco

T, Bistoni F.

Department of Experimental Medicine and Biochemical Sciences,

University of Perugia, Italy.

The effect of in vivo and in vitro N-acetylcysteine (NAC) treatment on

destructive activity of macrophages against Candida from COPD patients has

been evaluated. Patients received NAC (600 mg) or placebo orally 3 times a

day for 15 days and bronchoalveolar lavage (BAL) fluid and peripheral blood

were collected before and at the conclusion of treatment. In our system,

NAC treatment was not able to modulate antifungal activity of alveolar

macrophages, peripheral blood monocytes (PBM), and polymorphonuclear

leukocytes. On the contrary, in vitro NAC treatment at appropriate doses

(10 micrograms/ml) significantly enhanced antifungal activity of PBM from

COPD patients. This phenomenon is mediated by augmented phagocytic activity

and phagosome-lysosome fusion. The lack of correlation between in vivo and

in vitro studies could be ascribed to differences in the intracellular

concentration of the drug that in vivo does not reach levels capable of

inducing macrophage activation. We speculate that in COPD patients who

undergo long-term NAC treatment, appropriate schedules and doses of the

drug could augment resistance against microbial infections which are often

life-threatening in these patients.

Publication Types:

* Clinical Trial

* Controlled Clinical Trial

PMID: 8131544 [PubMed - indexed for MEDLINE]

J Autism Dev Disord 1999 Oct;29(5):426-7 Related Articles, Books, LinkOut

Auditory dysfunction in autism: a submicroscopic form of Wernicke's

encephalopathy?

Simon N.

Publication Types:

* Letter

PMID: 10587890 [PubMed - indexed for MEDLINE]

Mt Sinai J Med 2001 May;68(3):216-8

Wernicke's encephalopathy in a non-alcoholic man: case report and

brief review.

Munir A, Hussain SA, Sondhi D, Ameh J, Rosner F.

Department of Medicine, Mount Sinai Services at Queens Hospital

Center, Jamaica, NY 11432, USA.

Wernicke's encephalopathy, a serious neurological disorder caused by

thiamine deficiency, is most commonly found in chronic alcoholics. We

present a typical case of Wernicke's encephalopathy in a non-alcoholic man.

Our patient presented with altered mental status, slurred speech, fever,

vomiting and headache of one-week duration. An infectious etiology of the

symptoms was ruled out by spinal fluid cultures. The patient improved

dramatically within 24 hours of administration of thiamine.

PMID: 11373696 [PubMed - indexed for MEDLINE]