We are talking about the Candida genus, not just one particular species.

If you want to play it that way then you also have to admit that not all species of Candida respond the same to pH. Candida albicans, the most common species we deal with still thrives and becomes pathogenic in an alkaline environment.

There are many problematic species and who is to say one's problems are not caused by several species?

And again, different species can react differently to pH. You presented a study showing their results on only two of how many species of Candida? How many other species of Candida thrive in an alkaline pH like Candida albicans?

"The changing face of candidemia: emergence of non-Candida albicans species and antifungal resistance."

http://www.ncbi.nlm.nih.gov/pubmed/8678081

RESULTS:

Four hundred twenty-seven consecutive patients were enrolled. The frequency of candidemia due to non-C. albicans species significantly increased in each hospital throughout the 3.5-year study period (P = 0.01). Thirteen percent of candidemias occurred in patients who were already receiving systemic antifungal agents. Candidemias developing while receiving antifungal therapy were more likely caused by non-C. albicans species than by C. albicans species (P = 0.0005). C. parapsilosis and C. krusei were more commonly seen with prior fluconazole therapy, whereas T. glabrata was more commonly seen with prior amphotericin B therapy. Candida species isolated during episodes of breakthrough candidemia exhibited a significantly higher MIC to the antifungal agent being administered (P < 0.001).

CONCLUSION:

In this large scale study, the non-C. albicans species, especially T. glabrata, emerged as important and frequent pathogens causing fungemia. This finding has major clinical implications given the higher complication and mortality rate associated with the non-C. albicans species. The change in the pattern of candidemia might be partly attributed to the increase in number of immunocompromised hosts and the widespread use of prophylactic or empiric antifungal therapy. This is an ominous sign given the in vitro resistance of the non-C. albicans species to currently available antifungal agents.

Again, see my last comment.

Anyway, I have always believed that candida can mutate readily into different "species" within the body depending on its agenda.

Belief is far from proof.

The article you yourself posted would agree:

" We show here that sucrose-positive revertants of C. stellatoidea type II are readily isolated and that C. stellatoidea type II strains probably resulted from a mutation in the sucrase gene of C. albicans."

"Probably" is not proof either. And I ran across other articles that stated that C. albicans is not a variant of C. stellatoidea. So making such a claim without any evidence is a real stretch.

Besides, my article was orignally in response to another poster's study specifically citing albicans dimorphic pH threshold at pH 6.5. This may vary according to studies but I have already demonstrated to you that there is no significant difference between a pH of 5.5 to 7.0 on at least 4 other species of candida that grow hyphae (not sure if albicans was listed in that study or not). In other words, healthy colon pH of 5.5 to 7.0 is susceptible to hyphal dimorphism regardless of how much guar gum and rice bran some poor sap is consuming.

You are overlooking several important facts. One is that the change is pH dependent. The higher the alkalinity C. albicans is exposed to the more it is going to grow and develop dangerous hyphae. Secondly, overall pH of the intestines does not address pH of the acids by the flora. To help you understand this concept easier think about it this way. Let's say your stomach, depending on what is already in it is at a pH of 2. Then you drink a protein shake. Is the pH going to remain at 2? No, because of of dilution. Guess what, dilution also happens in the intestines. Still the flora can deliver a higher level of acidity to the Candida be being in direct contact.

If anything, you are making an argument against the use of antibiotics that destroy the gut flora.

Since you bring this up why don't you explain to all of us why killing off the acid forming bacteria with antibiotics leads to C. albicans overgrowth?

News flash: everyone knows this. But to take this a step further and use it as an argument against the effective anti-candida properties of alkalinity is absurd. As I have already stated, the HIGH alkalinity of healthy bile with a pH of 9.0 is ONE THOUSAND times more alkaline than colon pH of 6.0 and is devastating to candida colonies.

Wrong again. But since you brought this up how do you explain the fact that intestinal pH does not reach 9? I have in essence already given you the answer.

So is the highly alkalinizing diet of eating all green leafy vegetables. And this is easily proven both in the laboratory and through personal experience.

Green leafy vegetables do not promote bile release. Bile release is stimulated by fats. Green leafy vegetables provide fibers for the flora to ferment to produce beneficial acids.

And with regards to stomach pH: there are millions of chronically acidic americans who have low stomach acid levels. A healthy body-i.e. one that is not in acidosis- will have healthy stomach acid levels and be able to digest properly.

Do you even know how rare acidosis really is? Or what the few things are that can actually cause it?

There is no logical connection that can be drawn from this that would support your claim that "alkalinity causes candida to thrive". This is sheer nonsense.

Not if you read the research and understand how things actually work in the body. For example, how green leafy vegetables increase intestinal acids to control C. albicans.

As for liver flushing, which I have already thoroughly debunked you on, here are some basic facts that are readily observable to anyone with a decent modicum of intelligence:

You debunked me? LOL!!! In what universe? You simply made unfounded claims. I presented actual evidence to the contrary.

There is an overwhelming case for the intrahepatic reality of liver flush stones as well as an enormous body of anecdotal evidence on this site's archives.

No, there is not. There is a lot of evidence showing what people passed were primarily fecal soaps, which lab analysis also verified.

1) The idea that liver flush stones are somehow a product of the flush itself very quickly falls apart when you consider the occurrence of stones with a calcified shell being released in conjunction with the regular stones. When cut in half these stones are jade green. Andreas Moris's wife instantly cured her acute back pain after releasing 100 of these such stones.

2) Oftentimes the stones are passed in conjunction with liver flukes and other parasites of intrahepatic origin, like in my case stones covered in mycelial candida.

3) Stones cease being released after the flushing is complete, accompanied with a cessation of symptoms associated with intrahepatic stones.

Intrahepatic stones are about as rare as acidosis and are seen almost exclusively in Asian countries as I also presented proof to.

4) Some flushes produce no stones; while many have reported releasing stones without flushing at all.

This does not make them gallstones or liver stones. They are fecal soaps as the evidence has shown.

5) The size and amount of the liver stones released are strongly correlated to the diameter range and ratio of the biliary duct network.

Not even close as I have already proven numerous times.

There are innumerable tiny stones often the size of a grain of sand released, with increasingly fewer quantities the larger the stone is, tapering off to about 1cm, the diameter of the common bile duct.

6) There is a progression to flushing, with improved digestion and cessation of ailments for a brief period followed by a return of ailments and reduction in digestion as the deeper stones progress forward down the biliary ducts and once again occlude bile flow. More stones are released after 6 weeks after a flush than after 2 weeks.

7) There are varying colors of stones released at the same time despite passing nearly clear water due to the purging effects of the epsom salt, and consuming clear oil in the flush drink. Stones stored in the liver from different time periods and composed of different materials are released at the same time. There are also different colors of stones passed from flush to flush.

8) People, such as myself, have passed stones immediately after consuming the flush mixture.

9) People have passed stones on the eve of the flush before taking any mixture.

10) People have passed stones during the apple juice preparation phase.

11) People have passed stones from coffee enemas.

12) People have passed stones from eating several avocados.

13) People have passed stones from drinking carrot juice after prolonged water fasts.

14) The time of passage through the gastrointestinal tract is insufficient for saponification and formation of stones due to the laxative effect of epsom salt. Contractions of the gallbladder are felt just minutes prior to releasing the stones.

15) Some stones are clearly observed to be comprised of smaller stones that have clumped together over time, correlating to the formation of intrahepatic stones where smaller stones from the smaller biliary ducts clump together with other smaller stones as the ducts merge together into a larger duct.

16) Some tubular formations are released with hollow centers resembling the tubular shape of biliary ducts.

17) There are direct physical sensations of stones leaving the liver and gallbladder and traveling down the intestines.

18) Upon releasing stones, there is permanently more room to breathe, and more room for the stomach to expand and comfortably hold more food.

19) Completely flushing the liver until no more stones are released is directly and strongly correlated to the cessation of longstanding symptoms associated with intrahepatic stones.

Considering all the above, it should be overwhelmingly evident to any reasonably thinking individual that the origin of the liver flush stones is indeed intrahepatic.

Now consider some of the counter arguments from the proponents of the fecal soap cult: "Fecal dye" accounting for the various colors of the stones (what about passing only clear water prior to passing stones?) ,"Undigested cellulose" accounting for tubular waxy formations with a hollow center (once again, what about the fast beforehand and the absence of intestinal debris?), "calcium oxalates from the carrot juice" accounting for calcified stones (this one has got to be the most ridiculous. Does anyone really believe that calcium from carrot juice can coat a liver stone with a hard white shell in the 20 seconds it takes to exit the intestines?).

The origin of the liver flush stones is indeed intrahepatic.