I don't know a lot about all the different forms of glucosamine but there is one form that I do know is helpful for candida sufferers because it prevents candida from adhering to mucosal lining and it promotes Bifidobacteria growth. That form is called N-acetyl-D-glucosamine (NAG for short). Here is a write-up I found on it:

N-acetyl-D-glucosamine (NAG) is a naturally occurring aminoglycan found in large concentrations in intestinal mucus, secretory IgA, and other immunoglobulins. Intestinal mucus plays a critical role in protecting the host by providing a mechanical and immunological barrier against toxins, antigens, and bacteria in the gut lumen. Studies have shown that NAG blocks the adherence of Candida albicans to the gastrointestinal mucosa in vivo in animals and stimulates the growth of beneficial Bifidobacteria in vitro.116,117 Studies indicate that a defect exists in the glycoconjugate composition of intestinal mucin in many patients with IBD.118,119 One clinical study found that NAG is deficient in the mucin of IBD patients compared to non-IBD controls. This appears to be due to a defect in the biosynthesis of NAG involving N-acetylation of glucosamine-6-phosphate to form NAG.120 NAG can be absorbed from the gut lumen and directly incorporated into glycosaminoglycans and glycoproteins of the intestinal mucosa.121

I found this info from a great webpage about healing leaky gut. The entire thing is fantastic. You can find it here:

http://naturalmedicinejournal.com/journal/2010-03/nutritional-protocol-treatment-intestinal-permeability-defects-and-related

JoshOp, Sorry to burst your bubble, but you are entirely factually incorrect with respect to both your perspective regards the pharmacology of N-Acetyl-D-Glucosamine with respect to Candida Albicans in vivo; and more importantly your recommendations that people avoid taking N-Acetyl-D-Glucosamine per orally, wherein the reality is the precise OPPOSITE of what you are erroneously saying here.

Here's where you went wrong:

1) RE: The first study to which you refer; namely: RESPONSE OF CANDIDA ALBICANS TO GLUCOSAMINE AND SOME RELATED COMPOUNDS | STEWART A. KOSER AND ILSE TRIBBY | Zoller Memtiorial Dental Clinic, and Department of Microbiology, University of Chicago, Chicago, Illinois | Received for publication May 10, 1961)

You clearly have not properly read the or understood the salient information regarding this study... The findings of this particular study reports an essentially INSIGNIFICANT difference between the growth of Candida in response to adminstration of N-Acetyl-D-Glucosamine as compared with adminstration of PLACEBO (GLUCOSE)... I reiterate, an essentially INSIGNIFICANT difference.

Furthermore, this particular study is OVER 50 YEARS OLD, wherein the Candida strains today, including Albicans, cannot be said to be identical, having evolved and/or mutated over the past HALF CENTURY.

And thirdly, this study was IN VITRO and NOT IN VIVO and hence is not valid. In other words, you cannot correlate an IN VITRO study and make conclusions that the same occurs IN VIVO.

The minimum that is required for any use or validity whatsoever is IN VIVO ANIMAL studies, but even with this it is not necessarily going to apply to HUMANS, but at least provides a modicum of scientific substantiation whereas IN VITRO studies do not.

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2) RE: The second study to which you refer; namely: Identification of an N-Acetylglucosamine Transporter That Mediates Hyphal Induction in Candida albicans

This is also an IN VITRO study, NOT IN VIVO, and hence is both invalid and by no means whatsoever can be considered scientific substantiation.

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3) RE: The third study to which you refer; namely: Mechanisms of adherence of Candida albicans to cultured human epidermal keratinocytes. (Infect Immun. 1993 Nov;61(11):4560-8.)

“The most potent competitive saccharide inhibitors of C. albicans adherence to human keratinocytes were the amino sugars D-(+)-glucosamine”.

Again, you clearly have not properly read the or understood the salient information regarding this study either... The findings of this particular study reports precisely the OPPOSITE of what you have erroneously stated; wherein THIS is what the study reports: “The most potent competitive saccharide inhibitors of C. albicans adherence to human keratinocytes were the amino sugars D-(+)-glucosamine”. In other words this confirms that N-ACETYL-D-GLUCOSAMINE substantially prevents CANDIDA from affixing to the intestinal lining, and thereby the spread of the pathogen, which is a GOOD THING.

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4) There exists overwhelming evidence via IN VIVO studies that demonstrate that N-ACETYL-D-GLUCOSAMINE in fact has the PRECISE OPPOSITE effect that you are erroneously stating... Wherein, not only does N-ACETYL-D-GLUCOSAMINE substantially prevent CANDIDA from affixing to the intestinal lining but also equally substantially reduces its spread both systemically and otherwise. See HERE for example, where this study (one of numerous) is both comparatively RECENT and IN VIVO:

"N-ACETYLGLUCOSAMINE PREVENTED THE ADHERENCE OF CANDIDA ALBICANS TO GASTROINTESTINAL TRACT... SYSTEMIC SPREAD [OF CANDIDA ALBICANS] WAS REDUCED WITH A SINGLE DOSE"

(Microbios. 1991;67(271):95-105. Protection against Candida albicans gastrointestinal colonization and dissemination by saccharides.)