There is a very persistent myth that Candida albicans cannot survive a high (alkaline) pH. The fact is that C. albicans can survive very acid to extremely alkaline pH. The primary difference is the form it takes on dependent on the pH. At a low (acidic) pH C. albicans remains in a less pathogenic yeast form, and its growth is inhibited. When C. albicans is exposed to a high (alkaline) pH it promotes the formation of its hyphal growth. This hyphal growth allows C. albicans to not only become pathogenic, but also to allow it to invade deep in to tissues and to promote organ damage. This hyphal growth is inhibited at an acidic pH of 4 or below reducing tissue invasion and damage. I have compiled some research from non-commercial sites to prove these facts. The growth of C. albicans in an alkaline environment, as well as an acidic environment in a pH range of 2 to 10:
"Upon response to environmental stimuli C. albicans can switch between yeast-like and filamentous, hyphal growth. This allows C. albicans to generate niche specific responses, form biofilms, adhere, and invade epithelial tissues. "
It is this switch to the hyphal growth, from alkalinity, that allows C. albicans to become pathogenic by more readily invading tissues:
Hyphal growth has been shown to be inhibited at the acidic pH of 4 in all strains of C. albicans showing that an acidic pH helps to prevent C. albicans from being pathogenic. An alkaline pH on the other hand promotes pathnogenesis of C. albicans as it promotes hyphal growth. The article from the following link points out what I have been trying to explain to people for decades. Stomach acid helps to control pathogen growth, including Candida. The same applies to the skin, which is normally slightly on the acidic side. When the pH is raised to the alkaline side candidiasis of the skin is promoted.
"In tissue samples from mucosal surfaces with a non-acidic pH, such as the tongue, oesophagus, intestine, and most skin areas, filamentous forms of C albicans predominated, and most of them exhibited both 1H4 immunostaining and an invasive phenotype (fig 3A ). In internal organs having a non-acidic pH (liver, lung, heart, and thyroid) from patients with systemic candidiasis, variable numbers of yeast cells were found, together with hyphae or pseudohyphae in virtually all cases. In these tissues, both yeast and filamentous forms showed strong 1H4 immunoreactivity (fig 3B , C). In contrast, in those tissues with an acidic pH, such as the stomach and collecting ducts of the kidney, the predominant form of C albicans was the blastospore (yeast). Interestingly, in these locations yeast cells essentially showed no 1H4 immunoreactivity (fig 3D , E). However, when adjacent tissue invasion was present, hyphae or pseudohyphae were the predominant form."
"The ability to undergo transition from the yeast to the hyphal form appears to be crucial in the pathogenesis of invasive candidiasis. 4– 6 Both yeast cells and hyphae are found in infected tissues and contribute to pathogenesis. Yeast cells are better suited for rapid haematogenous dissemination, but together with hyphal elements they are also capable of breaching epithelial and endothelial barriers to cause extensive organ damage. 4 During the infectious process, yeast cells and hyphae may encounter different microenvironments within the host. At acidic pH, C albicans grows mostly in the yeast form; at an alkaline pH, it grows primarily in the filamentous form. 2, 6, 7 Gastric acid provides an effective barrier to most microorganisms (normal gastric pH values are 1–3.5). In contrast, achlorhydria and the use of H2 antagonists, which raise gastric pH, have been found to be associated with a higher proportion of invasive gastric candidiasis. 17 Similarly, although the skin is relatively inhospitable to fungal growth, 18 the experimental increase of skin surface pH yields more pronounced cutaneous candidiasis in human volunteers. 19"