Thursday, 16 March 2017

Gilbert's syndrome

Candida Overgrowth
Moderate amounts of candida (and other yeast) live in every one of us without causing any harm, but when given free rein to grow unchecked, e.g. by wiping out the surrounding bacteria with broad-spectrum antibiotics, candida can change into its fungal form and spore through the intestinal wall into the rest of the body. Once through, it rampages around the body producing a multitude of symptoms.
All it needs for Candida to invade your gut is for something to kill off the normal flora; the bacteria that aid digestion and protect the gut from yeast. Once the flora are damaged, yeast will invade. In ideal circumstances, Candida can double in quantity every half hour, so it takes very little time for it to populate a damaged intestine. Hormones, antibiotics, environmental toxins, heavy metals and poor dietary habits can all contribute or cause a yeast infection. Once in the gut, candida creates an environment that prevents the normal flora from repopulating. The lack of flora causes mal-digestion of certain sugars, carbohydrates, minerals and trace nutrients and leaves food to rot in the gut, creating an ideal environment for the Candida.
According to the conditions it finds, candida can exist in 3 forms; a budding, multiplying yeast, a hyphae form, which penetrates the gut wall in search of nutrition in the blood and as highly invasive spores, which penetrate the gut wall to be transported in the blood stream to other organs.
Once the yeast has overgrown the gut, malnutrition will result, in the form of vitamin and trace nutrient deficiencies. In addition, the constant presence of a pathogen will stimulate the immune system 24 x 7 x 365, eventually causing immune deficiency (as found in CFS) and severe fatigue. Victims will experience a multitude of symptoms caused by malnutition, an impaired immune system, toxins from the yeast's metabolic processes and from the physical presence of the yeast."
Yeast make a number of chemical compounds which are then picked up and absorbed into the body. These compounds are quite toxic to the nervous system. These compounds include toxic alcohols and aldehydes, as well as the powerful nervous system poison hydrogen sulfide (editor's note: this is a totally different substance than hyrodgen sulfate). Alcohols depress the nervous system and at least some aldehydes are anesthetic agents, which of course put the brain to sleep. These chemicals slow the brain down so that the brain no longer works correctly. These chemicals should be cleared by the liver so that these chemicals never reach the brain.
Candida mainly exists in two forms: a round yeast that remains in the colon and is actively reproducing and the other in its fungal form that 'eats' through the intestinal wall and travels via the blood to any site in the body. Sugar (in many forms) activates candida metabolism and its by-products are neurotoxins (toxins that damage or destroy nerve tissue) such as formaldehyde, and alcohol. The nervous system can become deranged with candida due to specific neurotoxins. Autism is one example of this. Metabolites of candida are found in urine samples of children with autism. Specific bacteria and fungi migrate from the large to small intestines to break down undigested carbohydrates. Candida is also known to impair immune functioning. Approximately 80% of our immune system lies within the intestinal walls. What you do to your intestines directly affects your 'immune' system. The immune system will respond to candida and its by-products along with food molecules that escape into the bloodstream by secreting histamines causing classic symptoms of allergies and intolerances.
Occasionally, Candida overgrowth occurs throughout the body including the liver and blood. Once in the blood, the fungus can be carried anywhere in the body resulting in a myriad of health problems including frequent urinary tract infections, respiratory problems, gastrointestinal and liver problems, food allergies, decreased immunity, frequent or chronic fungus infections of the skin and nails, and weight gain. This condition is referred to as Systemic Candidiasis (also known as candidosis and moniliasis.)
Note: This doesnt match at all, while the other ones do quite well.
REFERENCE: Wikipedia - Candidiasis
Candidiasis, commonly called yeast infection or thrush, is a fungal infection of any of the Candida species, of which Candida albicans is probably the most common.
Yeast organisms are always present in all people, but are usually prevented from "overgrowth" (uncontrolled multiplication resulting in symptoms) by naturally occurring microorganisms... However, when it gets out of balance with the other "normal flora", such as lactobacilli, an overgrowth and symptoms can result. Pregnancy, the use of oral contraceptives and some antibiotics, and diabetes mellitus can lead to an increased incidence in yeast infections.
In immunocompromised patients, the Candida infection can become systemic, causing a much more serious condition, fungemia.
REFERENCE: Wikipedia - Fungemia
Fungemia is the presence of fungi or yeasts in the blood. It is most commonly seen in immunosuppressed or immunocompromised patients with severe neutropenia, oncology patients, or in patients with intravenous catheters.
The diagnosis is complicated, as routine blood cultures have poor sensitivity. Treatment involves use of antifungals, eg. fluconazole or amphotericin.
The two most important risk factors are:
• Use of broad-spectrum antibiotics
• Colonization by fungi (see eg. candidiasis)
The most common pathogen is Candida albicans, causing roughly 70% of fungemias, followed by Torulopsis glabrata with 10%, and Aspergillus with 1%. However, the frequency of infection by T. glabrata, Candida tropicalis, C. krusei, and C. parapsilosis is increasing, especially when significant use of fluconazole is common.

Symptoms of Candida
Common symptoms of Candida
A minority of suffers have numerous symptoms; the vast majority have thrush + a few others; not every sufferer has thrush.
Group 1: The damage to the intestinal wall allows undesirable toxins to permeate into the bloodstream. This condition called ‘leaky gut syndrome' often leads to:
• food allergies and intolerances
• migraines
• foggy brain
• muscle aches
Group 2: Once through to the rest of the body, candida has the ability to disrupt the endocrine system causing symptoms such as:
• thrush
• cystitis
• menstrual irregularities
• joint pains
• asthma
• hayfever
• sinusitis
• fungal infections of the nails/skin e.g. athlete's foot
• weight gain or weight loss
• ear infections
• chronic tiredness
• allergies
• sensitivity to perfume, tobacco smoke and petrol
Group 3: Symptoms in the intestines include:
• bloatedness
• flatulence
• diarrhoea and/or constipation
• itchy anus
In addition, candida involvement has been implicated in some cases of other illnesses e.g. ME/CFS, Endometriosis.
Candida leads to brain fog because having systemic candidiasis means you're constantly drinking alcohol, as yeasts convert sugars into alcohol. This also congests the liver, another major co-factor in brain fog. If the liver, the filter for blood, is congested, it cannot take toxins out of the bloodstream fast enough. These toxins will pass the blood-brain barrier of the brain and deplete the brain of oxygen and glycogen.
Candida yeast ferments dietary sugars into liver-toxic acetaldehyde in the process of turning sugar into energy. Candida also appears to increase gut and urinary levels of ammonia, another liver toxin.
Candida overgrowth can produce a large number of symptoms. Among them are headaches, migraines, bad breath and rectal itching. Mood swings, canker sores and persistent heartburn. Muscle and joint pain, numbness and tingling sensations in the face or extremities.
Also acne, night sweats, sore throat, nagging cough and clogged sinuses. PMS and thrush; a yeast infection of the mouth causing a burning tongue and white spots on the tongue and in the mouth, also cystitis and fungal infections of the skin and nails. Kidney and bladder infections, arthritis, flatulence (gas) gastritis, diarrhea, and chronic constipation. Colitis and ulcers in the digestive tract, leaky gut syndrome, female disorders; including sterility, fibrosis or pregnancy problems and vaginitis. Plus the Male disorders; prostatitis and impotence.
Further symptoms are allergies, hormonal imbalance, heart problems and poor memory / balance. Earaches and ear infections, asthma, sinusitis, fluctuation in blood sugar levels and meningitis.
These toxins represent a great strain on the liver. Which can no longer adequately detoxify the body, causing extreme fatigue and a general feeling of discomfort. Depression, hyperactivity and indigestion join the previously mentioned symptoms. These various symptoms can be caused by the fungus candida albicans. Which produces almost 100 different toxins.
What are the Signs and Symptoms of Candida Overgrowth?
Gas and Bloating
Some symptoms of Candida overgrowth are localized in the digestive system, other symptoms are found in different locations in the body. Just as bread rises from yeast due to carbon dioxide production from fermentation of carbohydrates, Candida also produces carbon dioxide in the intestine. The result is persistent gas and bloating.
Brain Fog
Another by-product of Candida is acetaldehyde, a poison that is converted into ethanol by the liver. As yeast multiplies and produces more acetaldehyde, the blood alcohol level rises, resulting in symptoms associated with drunkenness, including impaired mental and physical functioning.
As yeast moves through the holes in the mucosal barrier and travels throughout the bloodstream, it produces such disorders as chronic ear infections and sinus infections. Physicians commonly prescribe antibiotics for fungal ear infections and sinus infections, which can make the condition worse by further destroying the good bacteria in the body. Candida overgrowth is also responsible for fingernail and toenail fungus and recurrent vaginal yeast infections.
Excess toxins produced by Candida can leave a person feeling lethargic and fatigued and sometimes with joint and muscle pain. Quite simply, the body must exert energy to cleanse itself, and when Candida is overgrown, the toxic load on the body increases. Sugar and carbohydrate cravings are a common Candida symptom as yeast feeds on sugars. The result can be an increased desire for sugar, which in turn causes a rollercoaster effect in your energy.
Candida can cause autoimmune diseases due to the fact that Candida can increase the permeability of your intestinal lining, also known as "leaky gut syndrome." With leaky gut, large undigested food molecules can enter your bloodstream which the body recognizes as a foreign material. When this occurs, the immune system attacks the food. The immune response involves making antibodies, which are the equivalent to the immune system's memory. The next time the same type of food enters the body, the immune system remembers and attacks again. The result is a sudden food allergy or sensitivity to commonly eaten foods. Toxins made by candida also signal an immune response to produce antibodies. An autoimmune disorder occurs when the immune system reacts with a hyperactive response to the digestive process and the toxins within it. The hyperactive immune system begins to attack the body's own tissues. There are about 80 known autoimmune diseases. Among these diseases are: rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome, Chrohn's disease, diabetes, Lupus, and multiple sclerosis.
Following are a few classic symptoms of candida overgrowth:
Gastrointestinal: indigestion, gas, bloating, inflammatory bowel diseases, diarrhea, constipation, heartburn, bad breath and thrush (coating on tongue).
Physical: numbness, burning or tingling; painful, swollen, stiff joints; muscle aches and tension, nasal congestion, chronic headaches, blurred vision, shortness of breath, chest pains, dizziness, sinusitis, and chemical sensitivity.
Mental/Emotional: depression, mental confusion, irritability, insomnia, nervousness, anxiety, disorientation, impaired decision making, low energy, fatigue, hyperactivity, chronic ear infections and poor memory.
Skin: white fungal skin patches like dandruff, acne, athlete's foot, anal itch, diaper rash, psoriasis, dermatitis, finger and toenail infections, unpleasant body or hair odour, genital touching in infants and young children, skin rashes and behavioural problems.
Sexual: vaginitis, discharge, itch, bladder infection, menstrual irregularities, pain, cramps, lowered libido, infertility, impotency, prostate problems.
Urinary: frequent urination, burning, fluid retention and edema.
Weight problems, vaginal yeast, athlete's foot, scalp problems such as dandruff, nail fungus, joint inflammation, poor immune response, headaches, allergies, shingles, oral thrush, canker sores, excessive sneezing, poor memory, brain fog, tooth plaque, hemorrhoids, throat mucous, and skin eruptions like acne, are all connected with Candida overrun… And "Sleep" in the corner of the eye indicates a Candida problem, so does a coated tongue.

Most allergies can be eliminated with the elimination of Candida overgrowth. The waste products of Candida flood the lymph system with more toxins than it can handle, and the body develops allergies. Candida overgrowth drastically reduces digestion, allowing undigested food into the blood stream. This undigested food causes an immune response, the making of an allergy.

Many reoccurring sinus problems are Candida overgrowth. Toxic bowel from Candida leaks toxins into the sinus cavities. The body rids itself of these toxins with a "runny nose."

Headaches, particularly migraine, may be Candida. Bowels overrun with Candida form excess mucous as a protection. This causes a very toxic, dehydrated lymph system. The immune system's response is to build antigens that flood the lymph. Toxic dehydrated lymph will give you a headache.

My favorite symptom, bloating and gas, can come from Candida. When high glycemic foods are eaten, the Candida feasts. A by-product of this is gas, just like the making of beer. The bad breath and gas makes for interesting company, probably lets you know who your friends are, too.
Candida may cause gum problems by weakening the gum below the tooth line. As stated earlier, most excess plaque is Candida related. Toe fungus is Candida. Losing a toenail to fungus is like losing your teeth to it.
What are the symptoms of Candida Overgrowth?
The symtoms are many and are so varied and manifest as so many other problems that you would not believe that they can be caused by the same thing. Some symptons are listed below, if you only have more two or three of these symptoms on a regular basis then you may have a problem with candida overgrowth:
* Recurring headaches/ migraines.
* Rashes, itching skin.
* Thush - oral/vaginal.
* Abdominal bloating. Intestinal bloating can also be caused by 'swallowing air' and the simple cure is 'catch yourself doing it and stop it'.
* Recurrent indigestion.
* Dry mouth or throat, constantly having to clear throat when speaking.
* Joint pain.
* Brain fog, fuzzy thinking.
* Feeling 'blue', mood swings.
* Hangover symptoms after bread/cakes.
* Sinus problems.
* Athletes foot type fungal problems.
12) As touched on above, pioneering researchers believe that depression is another symptom of Candida overgrowth—or more specifically, the 80 plus poisonous toxins and neurotoxins that candida yeast can produce inside the body. It is this toxic waste that they believe to be the primary cause of depression, especially for the chronically ill. These toxins can mimic and interfere with many of the body's hormones. When this happens, feelings of intense depression may be induced.8,9,10
In addition to the toxins put off by the yeast itself, Candida also survives by manufacturing toxic substances from refined carbohydrates and sugars in the digestive system. Hypersensitivity to these Candida yeast toxins, the most harmful of which is acetaldehyde (a by-product of alcohol and the chemical that naturally causes a "hangover"), can lead to anxiety, depression and impaired intellectual functioning.

Causes of Candida Overgrowth
Contributory factors
The popular perception is that candida is the consequence of antibiotics usage.The medical profession dismisses this as fantasy, saying that antibiotics could not have that effect in a healthy individual. But it may be that antibiotics act as the ‘final straw' where health has already been compromised, most probably by one or more of the following:
• use of the contraceptive pill or HRT
• use of natural progesterone cream
• use of other steroids (hydrocortisone, prednisolone etc.)
• use of immuno-suppressive drugs
• repeated use of broad-spectrum antibiotics e.g. for acne
• dental mercury amalgam poisoning
• other heavy metal poisoning e.g. lead, cadmium
• chemical poisoning from the home, garden, workplace etc.
• hormonal changes e.g. puberty, pregnancy, menopause
• stress
There are many causes of candida growth. It is adversely affected by drugs (prolonged use of antibiotics promote overgrowth), vaccinations, steroids and birth-control pills; chemicals such as mercury and other toxic metals, pesticides, aspartame, MSG and perfumes; diet including sugars and refined carbohydrates, consistent alcohol consumption, nutritional deficiencies, overeating and refined, canned, smoked, preserved and fried foods.
Mercury is an antibacterial, yet, in concentrations lower than fatal to humans, bacteria are often encouraged. Health forms of candida, normally found in the mouth, mutate under the influence of the mercury and the destructive bacteria to become harmful varieties of Candida. Mutated Candida produces at least 79 toxins. Sugar activates candida metabolism and some of its by-products are neurotoxins such as formaldehyde, alcohol and acetlyaldehyde. One's nervous system can become confused during candida infestation due to specific neurotoxins. Candida converts the element mercury to methyl mercury which is 100 times more toxic.
Mononucleosis / Glandular Fever
The glandular fever/candida link is often put down to the body's inability to control the bacteria in the gut when the immune system is compromised and under stress. The medical profession dismiss the fact that this can happen with a viral infection such as glandular fever because it is a relatively minor infection.
Populations More Susceptible To Candida
SCIENCE: National Library of Medicine
Comparison of Candida albicans adherence to human corneocytes from various populations.

Epidemiological data indicate that patients suffering from diabetes, hypothyroidism, obesity, or following prolonged treatment with antibiotics, corticosteroids or oral contraceptives, have an increased tendency to develop cutaneous candidiasis. Since it is generally believed that attachment of microorganisms to host cells is an initial step in the evolution of infection, the aim of the present study was to investigate whether cells from susceptible individuals have increased capacity to bind the fungus. Corneocytes collected from the forearms of individuals of these susceptible groups were exposed in vitro to Candida albicans and adhesion to the cells was evaluated in comparison with adherence to cells from a non-susceptible population. Adherence in vitro was assayed microscopically and evaluated quantitatively by two parameters: 1) percentage of adherence - number of corneocytes with adhering yeasts on their surface, and 2) the total number of adhered yeasts. Results of the study revealed that the mean percentage of adherence and the mean total number of yeasts adhering to cells from individuals of the susceptible populations was twice as high as values in a healthy population. Statistical analysis of the data by Student's t-test indicated that the difference was significant (p less than 0.001).
In Short: Candida adheres twice as much to cells from individuals suffering from diabetes, hypothyroidism, obestiy, or following prolonged treatment with antibiotics, corticosteroids, or oral contraceptives.
SCIENCE: National Library of Medicine
Chronic mucocutaneous candidosis associated with hypothyroidism: a distinct syndrome?

Chronic mucocutaneous candidosis (CMC) is a rare, complex disorder characterized by chronic and recurrent candida infections of the skin, nails and oropharynx. In over 50% of cases there is an associated endocrine disease, the complex being described as the candida endocrinopathy syndrome. Inheritance of familial endocrine associated cases has been thought to follow an autosomal recessive pattern. In addition, autosomal recessive and autosomal dominant forms of CMC not associated with endocrinopathy have been described. We report a new syndrome in which there is vertical transmission of CMC within families associated with primary hypothyroidism. This suggests that the candida endocrinopathy syndrome can be subdivided into at least two types, one associated with hypoparathyroidism and/or hypoadrenalism which is inherited as an autosomal recessive trait, the other associated with hypothyroidism which is an autosomal dominant disease. We emphasize the importance of early and regular monitoring thyroid function in individuals with CMC and a need to provide appropriate genetic counselling to affected members.
In Short: 50% of people who develop recurrent candida infections of the skin, nails and oropharynx have endocrine disease, including hypothyroidism.

What Candida Feeds On
The yeast, Candida Albicans, became the most popular colon microbe in the 1980's and many people still pursue yeast-free diets in an attempt to treat "candida infection" and to solve bowel symptoms. Claims that candida overgrowth in the GIT cause ill-defined illnesses are probably not true. Candida populations are balanced by competitive microbes. Colon candida are fed by milk sugar and starches in the diet which reach the colon undigested, not free sugars in food which tend to be absorbed before reaching the yeast. The presence of other kinds of yeast or fungi in the diet has little or no effect on the growth of candida in the colon. On a food holiday, the food supply to the Candida and all other colon microorganisms is reduced and the population decreases. The use of an elemental nutrient formula, even with high glucose content, is associated with reduction or disappearance of candida in the colon.
Limited effect of refined carbohydrate dietary supplementation on colonization of the gastrointestinal tract of healthy subjects by Candida albicans
Infections due to Candida albicans occur readily in situations in which ample glucose is available. In mice, dietary refined carbohydrate supplementation leads to higher rates of Candida growth in the gastrointestinal tract and favors mucosal invasion.
No correlation between C. albicans counts in the specimens and the habitual uptake of refined carbohydrates was observed. A high-sugar diet did not increase the frequency of C. albicans–positive samples, the number of subjects positive for C. albicans in the mouth washes, or the concentration of candidal blastoconidia in the samples of the 28 subjects. However, in selected subjects with elevated counts of oral C. albicans, we observed an increase in fecal C. albicans counts in response to the diet.
Candida thrives on carbohydrates, preserved refined foods and mold. Also foods that contain yeast and gluten, a wheat bread protein... Symptoms often worsen in damp and or moldy places. Also after consumption of food products rich in yeast or carbohydrate (sugars and starches) or after eating any the foods that contain mycotoxins.

Estrogens & Candida's Fungal Mode
SCIENCE: National Library of Medicine
Binding and reactivity of Candida albicans estrogen binding protein with steroid and other substrates.
In this report recombinant estrogen binding protein (EBP1), isolated originally from Candida albicans as a result of its high affinity for 17beta-estradiol... It is shown that like OYE, the protein binds a variety of compounds with a phenolic structure, including 17beta-estradiol, and compounds with an alpha, beta-unsaturated keto or aldehyde structure.
Cellular and Molecular Biology of Candida albicans Estrogen Response
Candida albicans is the most common etiological agent of vaginal candidiasis. Elevated host estrogen levels and the incidence of vaginal candidiasis are positively associated. Elevated estrogen levels may affect host and/or fungal cells. This study investigates the effect of 17-ß-estradiol, 17-{alpha}-estradiol, ethynyl estradiol, and estriol on several C. albicans strains at concentrations ranging from 10–5 to 10–10 M. The addition of 17-ß-estradiol or ethynyl estradiol to C. albicans cells caused an increase in the number of cells forming germ tubes and an increase in germ tube length in a dose- and strain-dependent manner. The addition of 17-{alpha}-estradiol or estriol did not have a significant effect on germ tube formation by the cultured cells. Exposure to exogenous estrogens did not significantly change the biomass of any C. albicans culture tested. The transcriptional profile of estrogen-treated C. albicans cells showed increased expression of CDR1 and CDR2 across several strain-estrogen concentration-time point combinations, suggesting that these genes are the most responsive to estrogen exposure. Analysis of strain DSY654, which lacks the CDR1 and CDR2 coding sequences, showed a significantly decreased number of germ tube-forming cells in the presence of 17-ß-estradiol. PDR16 was the most highly up-regulated gene in strain DSY654 under these growth conditions. The cell biology and gene expression data from this study led to a model that proposes how components of the phospholipid and sterol metabolic pathways may interact to affect C. albicans germ tube formation and length.
In Short: Candida albicans grows more and longer germ tubes when exposed to 17-ß-estradiol or ethynyl estradiol.
SCIENCE: National Library of Medicine
The effect of estradiol on Candida albicans growth.
The size of colonies growing on Sabouraud's dextrose agar (SDA) supplemented with 1 microM beta estradiol (1,3,5[10]-estratiene-3,17B-diol) was compared to those growing without the estrogen supplement. Data (video pixel counts) were obtained by video capture and image analysis and revealed that yeast strains were not uniformly stimulated by estradiol. One estrogen-responsive strain was evaluated in a chemically defined medium to evaluate growth in the presence of 17-alpha and 17-beta isomers of estradiol. The beta isomer promoted more rapid growth of the test organism and resulted in greater biomass production than the alpha isomer. Understanding of the role of mammalian hormones as growth promoting signals may provide information on this organism's shift from saprophytic to commensal to pathogenic status in vivo. Strain variation in response to estrogen may provide an explanation for differences in virulence.
In Short: Some strains of candida albicans respond to beta estradiol, others do not. But importantly, this reveals terminology of the stages - saprophytic, commensal, pathogenic.
SCIENCE: National Library of Medicine
Genistein effects on growth and cell cycle of Candida albicans.
Microbial virulence is generally considered to be multifactorial with infection resulting from the sum of several globally regulated virulence factors. Estrogen may serve as a signal for global virulence induction in Candida albicans. Nonsteroidal estrogens and estrogen receptor antagonists may therefore have interesting effects on yeast and their virulence factors. Growth of C. albicans was monitored by viable plate counts at timed intervals after inoculation into yeast nitrogen broth plus glucose. To determine if increased growth of yeast in the presence of estradiol was due to tyrosine kinase-mediated signaling, we measured growth in the presence of genistein, estradiol or genistein plus estradiol and compared these conditions to controls, which were not supplemented with either compound. Unexpectedly, genistein stimulated growth of C. albicans. In addition, genistein was found to increase the rate of germination (possibly reflecting release from G(0) into G(1) cell cycle phase) and also increased Hsp90 expression, demonstrated by a dot blot technique which employed a commercial primary antibody detected with chemiluminescence with horseradish peroxidase-labeled secondary antibody. These biological effects may be attributable to genistein's activity as a phytoestrogen. In contrast, nafoxidine suppressed growth of Candida and mildly diminished Hsp90 expression. This study raises the possibility of receptor cross-talk between estrogen and isoflavinoid compounds, and antiestrogens which may affect the same signaling system, though separate targets for each compound were not ruled out.
In Short: LOOK AT THIS! Genistein stimulates growth of Candida albicans and increases the rate of germination. As a phytoestrogen (isoflavone) it's an activator of candida albicans! And those with Gilbert's have trouble processing estrogens, making an environment that encourages candida albucans growth. Also, investigate nafoxidine as a possible way to regulate this environment.

The Connection to Gilbert's Syndrome - What Candida Eats, We Provide
Candida can be caused to turn from yeast to fungal mode by stimulation of estrogens. This includes stimulation by genistein, the primary isoflavone found in soy. There MAY be a connection to GS in that two of the three UGT enzyme systems that work slow in us process estrogens, including genistein, meaning that they probably last in the system a lot longer than in other people. Estrogens also make fungal candida more able to survive higher and lower than normal temperatures in the body. Coumarins are also protective to candida, and are processed more slowly by those with GS.
SCIENCE: National Library of Medicine
Estrogen effects on Candida albicans: a potential virulence-regulating mechanism.
Three Candida albicans strains were tested in the presence of 17-beta-estradiol (10-6 M and 10-9 M) for increased growth and for enhanced survival during incubation at nonpermissive temperatures. All 3 test organisms showed increased growth in the presence of estradiol compared with estrogen-free controls. Likewise, all 3 strains, when treated with estradiol, survived incubation at 48 degrees C better than did controls. Cytoplasmic extracts were probed with an anti-hsp90 antibody, and results suggested that intracellular hsp90 was up-regulated in the presence of 10-9 M 17-beta-estradiol. The results were confirmed by reverse-transcriptase polymerase chain reaction with primers specific for C. albicans hsp90. A kinetic study revealed that peak hsp90 expression occurred within 2 h of exposure to 17-beta-estradiol. In addition, estrogen increased the amount of cdr1 (Candida multidrug resistance) mRNA compared with cells not treated with estrogen. Coumarin and phenol also up-regulated hsp90 and cdr1 mRNAs, indicating that the estrogen-sensing and -response systems in C. albicans may lack specificity.
In Short: Candida albicans were able to survive incubation at nonpermissive temperatures when in the presence of 17-beta-estradiol. Coumarin and phenol also had a similar effect. Note that Coumarin is processed by UGT1A7, part of the Gilbert's Syndrome mutation haplotype which operates at 17%, and phenols are processed by UGT1A6, operating at 50%, meaning these also promote a better environment for candida albicans. Could candida possibly have something to do with these genetic mutations?

Candida Then Affects Gilbert's Syndrome
I know from experience that candida can cause bilirubin levels to rise. Last summer when my candida got much worse (as I continued to eat complex carbs) my bilirubin rose from 1.8 to 2.5. Candida produces toxins which are basically like alcohol and very hard on the liver. You may not be drinking a drop of alcohol, but the candida will make sure your liver has to deal with it anyway. I felt hungover every morning before I sorted my diet out.

Testing for Candida
Some sites with tests and questionaires:
The biggest problem in proving the existence of Candida Related Complex in non-immune compromised people is that until very recently, there were no good tests for the condition. Everyone has Candida in their system and in small amounts it is harmless. It is only in larger amounts that Candida is harmful. Therefore it is tricky to test for Candida. Simply showing that Candida is present in a person's system is useless. What are needed are tests that show how much is present in the system. The IgA, IgG, and IgM are three tests which are somewhat reliable separately, and together have a good degree of reliability. The candida immune complexes test is even more reliable.
SCIENCE: National Library of Medicine
Rapid identification of Candida albicans by dot-enzyme immunoassay.
A highly sensitive and specific dot-enzyme immunoassay for the rapid identification of Candida albicans was developed using a murine monoclonal antibody (Mab), which adsorbed to cell surface-exposed determinants. This Mab reacted with 28 of the 28 C. albicans strains tested including the serotypes A and B and 2 C. stellatoidea. It did not react with 32 other isolates representing eight other Candida species commonly encountered in human materials. All the test could be performed in four steps in less than an hour. The yeasts were directly spotted on a strip of immunodyne membrane. Then the strip was incubated for 5 min. with the Mab, for 15 min. with a peroxidase-conjugate and for 30 min. with the enzyme substrate and 4-chloro 1 naphthol. This test proved useful for rapid and easy identification of C. albicans.
SCIENCE: National Library of Medicine
Evaluation of a newly developed down-flow immunoassay for detection of serum mannan antigens in patients with candidaemia.
A down-flow immunoassay has been developed to detect serum mannan antigens, and the test was recently marketed as the Unimedi Candida monotest. Using 251 serum samples from 105 patients with candidaemia, a comparison of the Unimedi Candida monotest with the Cand-Tec latex agglutination test and 2 microplate enzyme immunoassay tests (Platelia Candida Ag test and Unimedi Candida) was conducted. One hundred and seventy-five febrile patients without clinical and microbiological evidence of fungal infections and pneumocytosis were examined as controls. The Cand-Tec test had a sensitivity of 38% and a specificity of 82%. The sensitivity and specificity of the Platelia Candida Ag test, the Unimedi Candida and the Unimedi Candida monotest were 53 and 92%, 69 and 89% and 82 and 96%, respectively. The sensitivity of the Unimedi Candida monotest was significantly (P<0.01) higher than that of the Plateria Candida Ag test for diagnosing candidaemia caused by Candida parapsilosis. The beta-D-glucan assay had a high sensitivity of 95%, with a specificity of 84%. Of 74 patients with candidaemia whose sera were available before or on positive blood culture sampling, 29 (39%), 38 (51%) and 48 (65%) patients had antigenemia detected using the Platelia Candida Ag test, the Unimedi Candida and the Unimedi Candida monotest, respectively. The Unimedi Candida monotest seems to be a promising tool for the early diagnosis of invasive candidiasis, because the test was sensitive, simple, rapid (approx. 1 h) and cost-effective.
The Candisphere is a blood test that shows the toxic waste that the Candida is releasing into the blood. The toxic wastes detected can only be released by large amounts of harmful Candida and not by small amounts of normal Candida. This test helps us to determine what stage of Candida overgrowth the person is in.
This test was determined to be 90% accurate for Candida by the FDA. When combined with the CDSA test it gives us the most accurate view of a patient's level of Candida and the cause of it. As stated above, the CDSA also reveals what needs to be done to eliminate the cause of Candida in the digestive tract.

In the natural health field many substances have bean promoted as being able to reduce yeast Infection. I have found that they do create a reduction in symptoms, but cannot destroy a yeast overgrowth in a systemic case.
Both undecylenic and caprylic acid are poorly absorbed into the blood stream making them ineffective in systemic cases. They only eliminate OR destroy it in the intestinal tract and will leave behind the colonies that have traveled to other parts of the body.
Acidophilus is helpful with some Candida symptoms while it is being used regularly. It is supposed to replace Candida in the intestines. But it cannot regrow and replace Candida until enough Candida has been cleaned out and the intestines are cleaner!
Note: This test appears to have been discontinuned
Home Candida Test.
The Candida Saliva Test. First thing in the morning before having anything to eat or drink, get a clear glass and fill with water. Work up some saliva and drop a spittle on top of the water and observe. If in 10 minutes time the spittle is still sitting on top of the water then you most probably do not have a candiadiasis problem. If however the spittle spreads and breaks up or you see streamers going down into the water then you may well have an imbablence.
Medical Diagnostic Lab Tests For Fungus, Yeast, Candida, And Parasites
This page is about medical diagnostic lab tests that will discover "clinical" evidence of a fungus, yeast, Candida, or intestinal parasite infection. The following material is a survey of medical labs having specialty tests or a reputation for executing standard tests to actually find these organisms. Candida and other fungus and yeast infections are notoriously difficult to identify. Yeast infections, and in particular, intestinal Candida yeast infections (and systemic Candidiasis), can lurk for years with few overt symptoms that allow a diagnosis. Consequently, medical diagnostic lab tests that irrefutably identify a yeast infection are vital in order for your doctor to be convinced, and for you to receive proper treatment.
Although this web site is oriented to fungus and yeast infections, this section includes information on diagnostic testing for intestinal parasites since they occur commonly in conjunction with intestinal yeast infections.
Available diagnostic tests include tests of blood, stool, urine, saliva , and tissue or bodily fluid samples (for example, cerebrospinal fluid from a spinal tap, fluid irrigated from the lungs, etc.).
Blood tests include antibody tests that look for IgG, IgA, and IgM antibodies to a specific fungus or yeast, and PCR (Polymerase Chain Reaction) tests which discover the presence of DNA of the fungus or yeast. (PCR is a method of multiplying an infinitesimally small amount of DNA into a measurable quantity.) Whereas antibodies may be present even after the infection is cured, the existence of DNA is positive indication of a current infection -- the bug is actually there, floating around in your blood stream. PCR may also be used to identify a specific strain of bacteria, fungus, or yeast.
In addition, blood may be cultured to discover the presence of bacteria, fungus and yeast infections, although blood cultures are hard to grow, and most turn out negative. "Finding Candida by blood culture is considered the definitive test for systemic yeast infection. However, in one of the most intensive studies done (18), there was a very high incidence of false negatives using blood cultures for Candida. In children who really did have yeast invasion of their organs including brain, liver, or heart that was confirmed by autopsy, only 17% of the children's blood samples tested positive for yeast even though they had been tested repeatedly (an average of ten times) for Candida." (Quote from Dr. Shaw at Great Plains Lab.)
Stool tests include microscopic visual examination for parasites and yeast, and culturing for specific pathogenic bacteria and yeasts. Since stool may contain a great many varieties of bacteria, mainstream labs normally only conduct cultures to discover a particular and suspected bacterial pathogen, as requested by the doctor. Similarly, they do not culture for fungus and yeast. However, there are several specialized labs that perform comprehensive analyses of stool, including culturing for bacteria and yeasts.
There are widespread opinions expressed on the web that the mainstream commercial and hospital labs are not attuned to the problems of intestinal yeasts and parasites, and consequently these infections may go undetected despite the submission of numerous specimens. Therefore, there appears to be a consensus among alternative medical thinking expressed on the web that patients and doctors attempting to diagnose and identify the cause of suspected intestinal yeast and parasite  infections should steer stool analyses to labs that focus on these problems. Several of these labs are identified on this page.
Culturing for fungi and yeast is problematic – many are very slow growing (fastidious) – so fungal and yeast cultures usually require 4 weeks before the lab will call it negative. However, only a culture can show the sensitivity of a discovered pathogen to drugs, so unless a culture is performed the selection of the drug is an empirical choice. You can find selection criteria at the excellent DOCTORFUNGUS site.
A fungal antibody test is a blood test that shows either Positive or Negative, but only for the specific fungi or yeast  in the test. Basically, they put a drop of your blood serum, a drop of an antibody for the fungus or yeast being tested, and a drop of a "control" blood serum each into a separate spot in a Petri dish filled with a thin gel. (The antigen is the bad thing; the antibody is the good thing in the immune system that tries to kill the bad thing.) The control blood serum has a known quantity of the antigen (the fungus or yeast) being tested for and is used to ensure that the test was performed correctly – it should always show a positive reaction. The blood components and the antibody slowly diffuse through the gel (hence, it's an "immunodiffusion test"), and will meet in about 30 minutes. If the antigen and antibody are an exact match the antibody latches onto the antigen and precipitates out, forming a visible line. If a line shows up, the test is positive, if not, it is negative. A positive may be reported as an "identity", since it demonstrates that the antigen in your blood serum is identical to the antigen in the control blood serum.
The two major diagnostic labs in the U.S. are Quest Diagnostics and Labcorp and both offer a version of the fungal antibody test. The Quest test (single immunodiffusion) is qualitative only – it detects the presence of the fungal antibody but does not indicate the degree of infection; by contrast, the Labcorp test (double immunodiffusion) also indicates the amount of antibody present.
You can read more from IMMY (Immuno-Mycologics, Inc.), the manufacturer of the Quest test, at this description of their antibody test. There is a somewhat better description provided for the Candida test.  "Immunodiffusion tests are used for the detection of precipitating antibodies (primarily of the IgG and IgA classes) against antigens of C. albicans. The presence of precipitating antibodies indicates active or recent infection."
The Quest test number is 4077N, and the Labcorp test number is 091454. Each test suite only covers the most common pathogenic fungi as listed in the table. The Quest test includes Candida; the Labcorp test does not. A doctor does not need to specify the test number since he may not know which lab will be used – the doctor can simply order "fungal antibody test". However, if Candida is suspected, the doctor's order obviously must specify Candida to steer the request to an appropriate lab (e.g. "fungal antibody test with Candida"). Most labs, presumably including Labcorp, will send out to another lab to fulfill a request if they don't provide it themselves.
AAL Reference Laboratories provides a Candida-specific antibody test #2323 Candida Antibodies (IgG, IgM & IgA) with Candida Immune Complexes.  Immune complexes are other proteins floating in the blood in accompaniment with the antibodies. "The only laboratory test that has been proven by independent clinical studies to be effective for the detection and monitoring of Active Candida Overgrowth is the Candida Immune Complex Assay." Their reported rationale for measuring the Candida immune complexes in addition to the Candida antibodies is as follows:
Standard Candida antibody analyses are both sensitive and specific with the following benefits:
• Elevated IgM levels suggest active or recent infection.
• Elevated IgG levels suggest a past infection.
• Elevated IgA levels are seen in patients who have had localized mucosal Candida infections (i.e., vaginal or mouth).
Although these tests have applications to the physician for the above reasons, they have the following limitations:
• IgM antibodies are transient and therefore, present for only a short period of time.
• IgG antibodies persist for many years after the infection has been cured.
• Antibodies tests lack the specificity for a conclusive diagnosis of clinical candidiasis (active Candida overgrowth).
Why Test for Candida Specific Immune Complexes?
For many years, Antibody Assay Laboratories has provided Candida specific immune complex measurements to physicians. They have found it extremely useful in the diagnosis and treatment of patients with active Candida overgrowth (Candidiasis) for these important reasons:
• Elevated Candida Specific Immune Complexes establish the presence of Candida overgrowth
• Immune Complexes levels drop quickly when the Candida load is reduced
• Candida Specific Immune Complexes are useful in monitoring the effectiveness of treatment. (Candida Immune Complexes will be reduced if the patient has responded to treatment).
• Elevated Candida Immune Complexes correlates with clinical symptoms of Candidiasis or Candida Overgrowth
• Candida Immune Complexes levels decrease with patient improvement
Note: For maximum effectiveness, Antibody Assay Laboratories suggests to repeat the Candida Immune Complexes assay after three months of treatment or when symptoms subside.
Saliva Antibody Test: A laboratory in London, the Institute for Individual Wellbeing, has modified the standard blood serum antibody test to work from a saliva sample. Performing the test is still complex (see Candida Saliva ELISA Test on this link), and requires a professional lab environment, but collecting the sample should be easier than a blood draw with the presumed intent for the patient to collect their own sample and mail to the lab.
Saliva Antibody Test: Also see BioHealth Diagnostics Mucosal Barrier Function #304 discussed below. This is a comprehensive test that evaluates a number of conditions. It detects antibodies to yeasts, and aerobic and anaerobic bacteria, among others. The test kit can be sent directly to the patient.
Multiple laboratories perform an "organic acid" test on urine to detect metabolic byproducts of Candida and other pathogens that pass into the blood stream from the intestines and are discarded in the urine. Versions of this test are available from several sources, including Great Plains Labs, Metametrix Lab, the Biamonte Center, and JackTips (all discussed below). (We should point out that the Biamonte Center and JackTips are treatment organizations, not labs, and probably either use purchased lab kits or send the samples out to a qualified lab.) "Organic acid tests can analyze a much broader spectrum of health conditions by examining a large number of different types of metabolites. Intestinal dysbiosis can be a significant factor in many health problems. The Metametrix Dysbiosis Metabolic Marker Profile measures the byproducts of bacterial and yeast metabolism that are excreted in urine. The Dysbiosis Profile is particularly useful in detecting the presence of pathogenic microbial overgrowth and monitoring therapy." See the Metametrix publication and the Great Plains lab test description.
Urine Test: A urine test for systemic candidiasis, called the Bio-Screen 'Yeast Cult' test, is available from Advanced Nutrition, Broadway House, Tunbridge Wells, Kent, UK. TN1 1QU (Tel: 01892-542012). The reference for this is from Carol Mason in the UK. This is likely to be an organic acid test as just previously described.
In addition to the more common tests that have been described, there are a number of other tests to mention. Here is a listing provided by Cerodex Labs, a wholly owned subsidiary of IMMY:
Complement Fixation tests for antibody to:
• Histoplasma mycelial antigen
• Histoplasma yeast antigen
• Blastomyces A antigen
• Coccidioides antigen
• Aspergillus fumigatus antigen
Latex Agglutination tests
• Antibody detection:
• Histoplasma antibody
• Coccidioides ('IDTP') antibody
• Sporothrix schenckii antibody
• Antigen detection:
• Cryptococcus neoformans capsular polysaccharide antigen
Yeast Agglutination:
• Cryptococcus neoformans antibody
Due to the esoteric nature of these tests, one would presume (or hope) that the lab would make the determination of when the use of each is appropriate, rather than expecting the requesting physician to know exactly what to ask for.
The Candisphere test, once produced by IMMY and available through Cerodex, has been discontinued, presumably replaced by more effective tests (the immunodiffusion antibody tests discussed above). Candisphere was an Enzyme Immunoassay test (EIA) detecting antibody to Candida cytoplasmic antigens. The term Candisphere appears with some frequency on Candida associated web sites.
CHROMagar is a diagnostic test developed by French biologist Dr. Alain Rambach which causes specific pathogens to appear in unique colors as they grow in a Petri dish coated with the proprietary agar growth medium. The growth medium product CHROMagar Candida will not only allow the growth and detection of yeasts - like traditional media - but in addition, just by the color of the colony, will instantly differentiate various Candida species. For detection and differentiation of major Candida species by colony color:
• Candida albicans- green
• Candida tropicalis - steel blue
• Candida krusei - rose, fuzzy
The growth medium product CHROMagar Orientation, although primarily intended for the detection of urinary tract pathogens, also serves as a general nutrient agar for isolation of various microorganisms. For rapid detection and differentiation of pathogens, including gram negative and gram positive bacteria  - pathogens which are identified by unique colors include:
• E. Coli - red
• Klebsiella - steel blue
• Enterococcus - turquoise blue
• Proteus - brown halo
• Pseudomonas - yellow
• Staphylococcus - white
Distributors in the U.S. and elsewhere sell the liquid growth medium as well as prepared Petri dishes to diagnostic labs. Some of the labs listed in this report are likely to use CHROMagar as part of their testing suite.
AAL Reference Laboratories, Inc. provides a blood serum antibody test to detect intestinal permeability (Intestinal Permeability Evaluation #2330) (also see the above discussion of AAL's Candida blood serum Antibody test):
"There appears to be a relationship between intestinal Candida overgrowth and increased intestinal permeability. This occurs particularly in patients that have chronic unresponsive Candida overgrowth with persistently elevated Candida immune complexes, despite prolonged antifungal therapy. These patients may have casein (from milk) and/or gliadin (from wheat) antibodies. Therefore, we recommend that patients with Candida overgrowth should also be evaluated for intestinal permeability by measuring IgA & IgG to casein or gliadin, as well as Candida immune complexes. Conversely, patients with suspected intestinal permeability should have Candida immune complexes measured as well as antibodies to casein and gliadin.
"A recent study 11 has also shown that patients with chronic unresponsive Candida overgrowth and increased intestinal permeability, also have a reduction in leucocyte phagocytosis. It is suggested in this study that this reduction is secondary to free radical damage to the neutrophils. It is important to identify these patients with poor leucocyte phagocytosis, because they may benefit from increased antioxidant therapy.
"The treatment of these patients should be focused on resolving their bowel dysfunction and should include: antifungal measures, mineral supplements, and antioxidants. Initially, they should have casein and gliadin removed from their diet and then after six months of this regime casein and gliadin can be reintroduced. Retesting for casein and gliadin IgA and IgG antibodies should be performed in the next month to assess the current intestinal permeability status."
Other labs performing Intestinal Permeability tests include Great Smokies Lab, and the Do It Yourself Tests from JackTips.
I tested myself for estradiol, the most potent form of estrogen in the body, after eating a lot of soy for a day. Normal range for an adult male is 0-53, and mine was 20. I found out later that soy actually diminishes estradiol in the blood by about 25% by taking its place. That means my normal level may have been 28. But still well within range. The test did not measure genistein levels.
On the subject of candida - systemic candemia specifically - there was just approved this month a new safer drug for its treatment. It's called Eraxis. Existing drugs were extremely danerous to the liver and kidneys.
So my blood test for candida antibodies was negative. However, I've read that this test shows a lot of false negatives, and it wasnt the test they advertised, which gives numerical results - this one gave only positive/negative results. I've read that people have died from systemic candidemia and had nothing show up in this blood test. They also had my blood sitting around for 5 days before they tested it.

Treatments for Candida
Eraxis - A New, Safer Drug
SCIENCE: Quest Diagnostics
New Drug for Candida Infections (May, 2006)
When we hear “Candida infections” or candidiasis, we don’t normally think fatal but certain forms can be. In the case of blood infections caused by Candida (usually Candida albicans), the mortality rate is about 40 % and there are about 60 thousand cases annually in this country.
FDA recently approved the use of a new, novel drug called “anidulafungin” (Eraxis®). This drug can be used to treat all kinds of Candida infections including blood stream infections (candidemia), esophageal infections (candidiasis), abdominal abscesses, peritonitis and other types of infections.
The drug, which is administered intravenously, is well tolerated and the only adverse effects noted thus far have been mild diarrhea, headache and slight elevations in liver enzymes.
FDA Approves New Treatment for Fungal Infections
The Food and Drug Administration approved Eraxis™ (anidulafungin) to treat certain infections caused by Candida, a yeast-like fungus that can cause serious infections in hospitalized patients or patients with compromised immune systems.
"This product offers a new alternative therapy for several types of infections associated with Candida", said Dr. Steven Galson, director of the FDA's Center for Drug Evaluation and Research. "It is a helpful addition to the available antifungal medications that can be used in the treatment of these potentially serious fungal conditions."
Eraxis, a new molecular entity that has never been marketed in the United States, is an antifungal drug that is administered intravenously, and is used to treat Candida infections in the esophagus (candidiasis), blood stream (candidemia), and other forms of Candida infections, including abdominal abscesses and peritonitis (inflammation of the lining of the abdominal cavity).
The safety and efficacy of Eraxis was evaluated in clinical studies and Eraxis was shown to be safe and effective in the treatment of esophageal candidiasis, candidemia, and other Candida infections including abdominal abscesses and peritonitis.
Eraxis was generally well tolerated in clinical studies. The most commonly reported adverse events were mild diarrhea, mild elevations in laboratory tests of liver enzymes, and headache. Some patients experienced infusion-related reactions, most of which were mild. In a few patients with significant underlying medical conditions who were on multiple concomitant medications, there were reports of serious hepatic abnormalities.
Drugs (dangerous)
REFERENCE: Wikipedia - Amphotericin
Amphotericin B (Fungilin®, Fungizone®, Abelcet®, AmBisome®, Fungisome®, Amphocil®, Amphotec®) is a polyene antimycotic drug, used intravenously in systemic fungal infections.

Side effects
Very often a most serious acute reaction after the infusion (1 to 3 hours later) is noted consisting of fever, shaking chills, hypotension, anorexia, nausea, vomiting, headache, dyspnea, and tachypnea. This reaction sometimes subsides with later applications of the drug and may in part be due to histamine liberation. An increase in prostaglandin-synthesis may also play a role. Often the most difficult decision has to be made, whether the fever is disease- or drug-related. In order to decrease the likelihood and severity of the symptoms, initial doses should be low and increased slowly. The liposomal preperation obviously has a lower incidence of the syndrome. Acetaminophen, pethidine, diphenhydramine and/or hydrocortisone have all be used to treat or prevent the syndrome, but the prophylactic use of these drugs should be limited.
Nephrotoxicity (kidney damage) is a major issue and can be severe and/or irreversible. It is much milder when amphotericin B is delivered in liposomes (AmBisome). Electrolyte imbalances (e.g. hypokalemia and hypocalcemia) may also occur.
Increased liver enzymes and hepatotoxicity up to acute liver failure, several forms of anemia and other blood dyscrasias (leukopenia, thrombopenia), serious cardiac arrhythmias (including ventricular fibrillation), and cardiac failure have also been reported frequently. Skin reactions, including serious forms, are also possible.
From studies it appears that liposomal amphotericin B preparations exhibit fewer side-effects while having similar efficacy. Various preparations have recently been introduced. All of these are more expensive than plain Amphotericin B.
AmBisome is a liposomal formulation of amphotericin B for injection, developed by NeXstar Pharmaceuticals (acquired by Gilead Sciences in 1999). It is marketed by Gilead in Europe and licensed to Astellas Pharma (formerly Fujisawa Pharmaceuticals) for marketing in the USA, and Sumitomo Pharmaceuticals in Japan.
Fungisome is a liposomal complex of Amphotericin B and being the latest and cheapest addition to the lipid formulations of Amphotericin B has many advantages. It is marketed by Lifecare Innovations of India. Other liposomal formulations include Amphotec® (Intermune) and Abelcet® (Enzon Pharmaceuticals).
REFERENCE: Wikipedia - Fluconazole
Fluconazole is a synthetic antimycotic drug of the triazole class of compunds. The drug is sold under the brand name Diflucan®. It is used orally and intravenously to treat yeast and other fungal infections.
Contraindications and cautions
Male rats treated with 5 mg and 10 mg/kg weight respectively showed a higher incidence of hepatocelluar adenomas than expected. No data exists on human carcinogenity.
• Known hypersensitivity to fluconazole is an absolute contraindication.
• Fluconazole may infrequently cause severe or lethal hepatotoxicity. Liver function studies should be obtained regularly. Patients showing clinical signs of liver damage should be immediately withdrawn from the drug. Patients with preexisting liver disease should be treated with particular care.
• Some patients develop severe skin reactions (Steven-Johnson-Syndrome or toxic epidermal necrolysis) under treatment. Patients with HIV-infections are particularly prone. All patients should be carefully watched for development of any skin reaction and should be advised to discontinue the drug immediately if rash or other forms of skin reactions are observed.
• Fluconazole may cause rare cases of prolongation of the QT interval, leading to serious arrhythmias. Risk factors are preexisting prolonged QT interval, electrolyte imbalances including hypokalemia, low serum level of magnesium and hypocalemia. These patients should be treated with caution and the electrolyte imbalances should be corrected before therapy is initiated.
• GI tract: Nausea, dyspepsia, abnormal taste, abdominal pain, vomiting, diarrhea, and flatulence were reported in 5.3% of patients. In female patients receiving a high single dose treatment for vaginal infections, the incidence of these side-effects may be higher.
• Skin : Skin rash, diffuse reaction with eosinophilia, and pruritus were encountered in up to 5%. Also alopecia and exfoliative skin reactions (including Stevens-Johnson-Syndrome and Lyell's-Syndrome) were seen. The latter had been fatal in some patients.
• Liver, kidney, hematology : Some patients, particular those with AIDS or malignancies, developed increased liver enzymes, bilirubin, AP, BUN, serum creatinine, eosinophilia, anemia, and leukopenia including agranulocytosis as well as thrombopenia. Symptomatic hepatotoxicity (hepatitis, hepatic necrosis, jaundice, cholostatic hepatosis, and fulminant liver failure) including fatalities had been infrequent.
• Central nervous system : Frequently headache, less frequently vertigo and convulsions. Some of these side-effects might have been due to the underlying disease (cryptococcal meningitis). An acute psychotic (paranoid) reaction had been noted in one case of overdose.
• Heart : QT interval prolongation and torsade de pointes (a serious arrhythmia) may occur.
• Different Side-Effects : Anaphylactic reaction (including facial edema, angioedema, and pruritus). Hypokalema, increased triglycerides, and increased cholesterol had also been encountered.
Another drug Nizoral impairs the productions of ergosterol, a vitamin D like substance, which is vital to the integrity of the yeast cell membranes. This drug is difficult for Candidiasis patients to absorb because proper stomach acid is required to absorb it. Most patients are deficient in stomach acid. Yeast infections sometimes produce symptoms that make people believe they have excess acid.
Taking yeast medication like Diflucan or Nystatin can temporarily relieve symptoms, but unless measures are taken to repopulate the gut with friendly bacteria and correct whatever caused them to die off in the first place, the yeast will simply grow back, hence reports that while killing the yeast helps alleviate symptoms, the effect is usually only temporary.
SCIENCE: National Library of Medicine
Candidaemia and antifungal therapy in a French University Hospital: rough trends over a decade and possible links.
ABSTRACT: BACKGROUND: Evidence for an increased prevalence of candidaemia and for high associated mortality in the 1990s led to a number of different recommendations concerning the management of at risk patients as well as an increase in the availability and prescription of new antifungal agents. The aim of this study was to parallel in our hospital candidemia incidence with the nature of prescribed antifungal drugs between 1993 and 2003. METHODS: During this 10-year period we reviewed all cases of candidemia, and collected all the data about annual consumption of prescribed antifungal drugs RESULTS: Our centralised clinical mycology laboratory isolates and identifies all yeasts grown from blood cultures obtained from a 3300 bed teaching hospital. Between 1993 and 2003, 430 blood yeast isolates were identified. Examination of the trends in isolation revealed a clear decrease in number of yeast isolates recovered between 1995-2000, whereas the number of positive blood cultures in 2003 rose to 1993 levels. The relative prevalence of Candida albicans and C. glabrata was similar in 1993 and 2003 in contrast to the period 1995-2000 where an increased prevalence of C. glabrata was observed. When these quantitative and qualitative data were compared to the amount and type of antifungal agents prescribed during the same period (annual mean defined daily dose: 2662741; annual mean cost: 615629 ) a single correlation was found between the decrease in number of yeast isolates, the increased prevalence of C. glabrata and the high level of prescription of fluconazole at prophylactic doses between 1995-2000. CONCLUSION: Between 1993 and 2000, the number of cases of candidemia halved, with an increase of C. glabrata prevalence. These findings were probably linked to the use of Fluconazole prophylaxis. Although it is not possible to make any recommendations from this data the information is nevertheless interesting and may have considerable implications with the introduction of new antifungal drugs.
Note: It'd be interesting to see the actual numbers of people, maybe in percentages, with candidemia.
(about ThreeLac:) About 10% of people tell us they feel better very quickly, within weeks. Another 10% may take 4-6 months to get the overgrowth under control, but the vast majority we have heard from achieve dramatic improvement in about 2 ½ to 4 months. Every person is different, so please be patient with the process. When you feel you are ready to graduate back down in your dosage, go just as slowly (one packet at a time) as you did in the first place. If your symptoms start coming back, you're going down too soon.
2) An anti-estrogen like Chrysin may lower estrogen levels. Chyrsin is legal but is NOT intended to cure any diseases(*** remember I'm not a doctor ***).
• Candida binds with B vitamins, particularly vitamin B6 which interferes with the production of serotonin, melatonin, and other neurotransmitters
• Caprylic acid is a natural fatty acid that kills candida (1-2 grams with meals)
Molybdenum breaks down the formaldehyde produced by the candida so it is not so harmful to the liver.

Anti-Candida Diet
A Candida diet without antimicotics will simply cause the Candida to change form and send hyphae through the wall of the gut and into the underlying blood vessels in search of glucose, resulting in leaky gut syndrome. In leaky gut syndrome, food particles are then free to enter the blood circulation and trigger allergic reactions.
Candida therapy starts with eliminating its energy foods from the diet, killing the fungus with various remedies, cleaning the intestinal walls, rebuilding the intestines, rebalancing intestinal flora and strengthening the immune system.
Strategies for success:
1. Suppress or kill the yeast with anti-fungals. Garlic is one of the most potent antimicrobial agents along with oregano. Pau D'arco is an extract of the bark of a South American tree known to have potent anti-fungal properties.
2. Deprive or starve the yeast by diet modification. A simple approach is to remove refined simple sugars, milk/dairy foods, alcohol, melons, fermented foods and dried fruit.
3. Cleanse and rebuild the walls of the gastrointestinal tract.
4. Rebalance bacteria in the colon with beneficial bacteria.
5. Identify and avoid drugs, chemicals, foods and other allergens such as, insecticides and preservatives that you know trigger candida and its symptoms.
The way to deal with this is starve the candida by eliminating all sugar, yeast, gluten, dairy and complex carbs - rice, pasta, potatoes, starchy vegetables - and take a good probiotic (Nature's Biotics)...
People with GS tend to have blood sugar issues as well, so eliminating or minimising complex carbs is not a bad thing to do anyway.

Estrogen Metabolism
The Functional UGT1A1 Promoter Polymorphism Decreases Endometrial Cancer Risk
In humans, more than 18 functional UGTs have been isolated, and several have demonstrated significant reactivity toward estrogens and their metabolites, catecholestrogens (14, 15, 16, 17, 18, 19, 20, 21) . UGT1A1 is thought to play a major role in the metabolism of estradiol (E2) because a Crigler-Najjar patient deficient in UGT1A1 had a 70% decrease in the hepatic glucuronidation of E2 compared with liver microsomes from healthy subjects (18) . UGT1A1 also catalyzes the glucuronidation of hydroxylated metabolites of E2 and estrone (17)... A common variant in the UGT1A1 gene, designated as UGT1A1*28 [A(TA)7TAA], is known to decrease the level of gene expression (30 , 31) . Variability in the expression of the UGT1A1 protein resulting from this polymorphism may lead to important differences in estrogen biotransformation.
Interindividual variability in levels of conjugated estrogens, in the form of estrogen glucuronides, have been measured in urine, breast cyst fluid, and follicular fluid, suggesting that UGT enzymes have an effect on the inactivation and elimination of estrogens and their accumulation in target tissues (13 , 32 , 43 , 44) .
Glucuronidation of Catechol Estrogens by Expressed Human UDP-Glucuronosyltransferases (UGTs) 1A1, 1A3, and 2B7
Catechol estrogens are major estrogen metabolites in mammals and are the most potent naturally occurring inhibitors of catechol-amine metabolism. These estrogen compounds have been implicated in carcinogenic activity and the 4/2-hydroxyestradiol concentration has been shown to be elevated in neoplastic human mammary tissue compared to normal human breast tissue. Three human liver UDP-glucuronosyltransferases, UGT2B7, UGT1A1, and UGT1A3, have been shown to catalyze the glucuronidation of catechol estrogens and lead to their enhanced elimination via urine or bile.
The Monkey and Human Uridine Diphosphate-Glucuronosyltransferase UGT1A9, Expressed in Steroid Target Tissues, Are Estrogen-Conjugating Enzymes
Of the more than 30 endogenous substrates tested, both proteins show the highest activity on 4-hydroxyestradiol and 4-hydroxyestrone, followed by 2-hydroxyestradiol and estradiol. RT-PCR analysis demonstrate that UGT1A9 transcript is expressed in several tissues, which include the prostate, testis, breast, ovary, and skin of the monkey and humans. The expression of UGT1A9 in extrahepatic estrogen-responsive tissues, and its high activity on estrogens is consistent with this enzyme having a role in estrogen metabolism.;2000/27/113
Chapter 6: Estrogen Metabolism by Conjugation
Conjugation of parent estrogens to sulfate and glucuronide moieties; of catechol estrogens to methyl, sulfate, and glucuronide conjugates; and of catechol estrogen quinones to glutathione conjugates all represent potential "detoxification" reactions that may protect the cell from estrogen-mediated mitogenicity and mutagenesis.
Estrogens exert biologic responses in steroid hormone-responsive cells largely via interaction with ERs, members of a superfamily of nuclear hormone receptors that act as ligand-activated transcription factors (5). There are two known ER subtypes, ER{alpha} and ER{beta} , which share similar estrogen affinities but have dissimilar expression patterns and response to antiestrogens (5–7). The two most potent endogenous estrogens, estrone and 17{beta}-estradiol, are both ligands for the ERs, although those receptors have higher affinity for 17{beta}-estradiol than for estrone and it is 17{beta}-estradiol that is believed to be the predominant endogenous activator of ER-mediated cellular processes (5). The most abundant circulating estrogen, however, is the sulfate conjugate of estrone (8,9).
Biologic Role of Estrogen Conjugation
The endogenous formation of estrogen conjugates has long been recognized as a major route of estrogen metabolism (17). Both endogenous and synthetic exogenous estrogens are extensively biotransformed to estrogen conjugates in humans (Fig. 1Go) (2,18). The most abundant circulating estrogen conjugates are the sulfates, followed by the glucuronides. It is important to note that conjugated estrogens are not appreciable ligands for the ERs; thus, they do not promote ER-mediated activity (2). Intuitively, it was initially assumed that sulfate and glucuronide conjugation of estrogens represented a pathway resulting in less active, more polar, and more readily excreted estrogenic compounds. It is now appreciated, however, that estrogen sulfates actually exhibit a much longer half-life than do the parent estrogens (2,8,11). Estrone sulfate is the most abundant circulating estrogen, at concentrations approximately 10-fold higher than unconjugated estrone (8). That finding, as well as increasing knowledge about the transport and subsequent desulfation of estrogen sulfates, has led to a widely held belief that sulfated steroid hormones serve an important biologic role as steroid hormone precursors, particularly for steroid hormone-responsive tissues (2,9). An increasing body of scientific data supports the hypothesis that sulfation and desulfation of estrogens may well represent an endogenous system important in the regulation of biologically active steroid hormones in target tissues (10,11). Specifically, it is currently hypothesized that inactive estrone sulfate is transported to target tissues via the circulatory system, taken into target cells, most likely by organic anion transporters, enzymatically hydrolyzed to estrone by intracellular membrane-bound steroid sulfatase (arylsulfatase C), and hydroxylated to active 17{beta}-estradiol via catalysis by 17{beta}-hydroxysteroid dehydrogenases (2,11,18,19). 17{beta}-Estradiol activates the ER via ligand binding and initiates a number of downstream ER-mediated events—most notably related to transcriptional activation of those genes that contain DNA sequences that bind and respond to activated ERs (5,18).
Enzymes responsible for the glucuronidation and deglucuronidation of estrogens are also expressed in a variety of human tissues, including the breast (24,25). Estrogen glucuronides have received much less attention, however, than have the sulfate conjugates as steroid hormone precursors, most likely because they are less abundant and more readily cleared from the body (2).
Biochemistry of Estrogen Conjugation
Sulfation. Sulfate conjugation of estrogens is catalyzed by several members of a superfamily of cytosolic sulfotransferase (SULT) enzymes (27,28). SULT enzymes catalyze the transfer of SO3- from 3'-phosphoadenosine-5'-phosphosulfate, the enzymatic cofactor, to, in the case of estrogens, phenolic acceptor groups (28). Cytosolic SULTs are active as homodimers. Sulfation of estrone and 17{beta}-estradiol occurs at the 3-phenolic group of the steroidal A ring (Fig. 1Go). Estrogen SULT activity has been demonstrated in a variety of human tissues, including liver, small intestine, kidney, placenta, uterus, adrenal gland, and breast (29–33). The level of estrogen SULT activity in the human liver is high, and this activity is believed to contribute significantly to the high circulating levels of estrone-3-sulfate (29,30). Although from a quantitative perspective, sulfation of estrogens in the liver is probably the most important overall estrogen-conjugating activity in the body, sulfation of estrogens in steroid target tissues, including the breast, has also been demonstrated and may well be important in affecting the biologic activity of estrogens within those tissues (2,11).
Glucuronidation. Estrogen glucuronidation is catalyzed by several members of a superfamily of microsomal UDP-glucuronosyltransferase (UGT) enzymes (25,37). UGTs catalyze the conjugation of UDP-glucuronic acid, the UGT cosubstrate, to a variety of endogenous and exogenous aglycones, including steroid hormones (38). Whereas estrogens are sulfated predominantly at the 3 position, glucuronidation can occur at either the 3 or 17{beta} hydroxyl group of steroidal hormones, with the 17{beta} position being the apparent predominant site of glucuronidation for 17{beta}-estradiol (Fig. 1Go). Glucuronidation of estrogens renders those molecules less lipophilic and more readily excreted in both urine and bile. 17{beta}-Glucuronides of estradiol are known to induce cholestasis, putatively via interaction with hepatocyte canalicular membrane efflux transporters such as MDR1 and MRP2/cMOAT (39,40). Steroid hormone glucuronidation has been observed in human liver, biliary epithelium, kidney, gut, prostate, ovary, and breast (25,26,38).
Molecular and Cellular Aspects of Estrogen Conjugation
There are a surprising number of SULT and UGT isoforms capable of contributing to the conjugation of estrogens. Those isoforms are often expressed in a tissue-specific manner and are often under specific regulatory control. Furthermore, a number of those conjugative enzymes are encoded by genes known to harbor common genetic polymorphisms. These factors help explain many of the complexities of estrogen conjugation—and this knowledge allows us to probe estrogen conjugation reactions in a systematic fashion.
Glucuronidation of estrone and 17{beta}-estradiol appears to be catalyzed by several members of the UGT1 family. Thus far, recombinant human UGTs 1A1, 1A3, 1A4, 1A8, 1A9, and 1A10 have all been shown to catalyze the glucuronidation of estrone and/or 17{beta}-estradiol (Table 1Go) (25,26,56–60). It is interesting to note that, for some human recombinant UGT isoforms, there appears to be selective affinity for estrone or 17{beta}-estradiol as substrate. For example, UGTs 1A1 and 1A4 exhibit activity toward 17{beta}-estradiol but not toward estrone, whereas UGTs 1A9 and 1A10 have been reported to catalyze the glucuronidation of both of these estrogens (25,26,56,58,60). Activity for UGTs 1A8 and 1A3 toward estrone has been reported, but the activity of those isoforms toward 17{beta}-estradiol has apparently not been evaluated (57,59).
UGT1A1 is expressed in human liver, colon, and biliary epithelium (gallbladder) but not in stomach (60). UGT1A3 has been reported to be expressed in human colon, biliary epithelium, and liver, but the level of expression in liver varied significantly between individuals and was fivefold to 10-fold less than the level of UGTs 1A1 and 1A4 (57,60). UGT1A4 is expressed in human liver, colon, and biliary epithelium but not in stomach (60). UGT1A8 appears to be expressed specifically in human intestinal tissues (59,60). UGT1A9 is expressed in human prostate, testis, breast, ovary, skin, skeletal muscle, stomach, small intestine, colon, liver, and kidney but not in biliary epithelium or stomach (25,60). UGT1A10 is expressed in colon, biliary epithelium, and stomach but not in liver (60).
As previously noted, the capacity for estrogen conjugation and, specifically, glucuronidation is known to vary widely in the human population (51). That observation raises the possibility that genetic variation may exist in the UGT isoforms that contribute significantly to estrogen glucuronidation. A functionally significant common polymorphism in the promoter sequence of the UGT1A1 gene has been described and well characterized (61–63). That polymorphism is a variable length (TA)n TAA repeat in the functional TATA box upstream of exon 1 of the UGT1A1 gene. The wild-type allele is defined as n = 6. Allelic variants identified to date include n = 5, 7, and 8 (63). In vitro studies utilizing reporter constructs driven by allelic variants of the UGT1A1 promoter (63) have shown that promoter activity appears to decrease with increasing n. Furthermore, clinical association of the most common variant (n = 7) with a relatively poor ability to glucuronidate bilirubin (Gilbert's syndrome), as well as the chemotherapeutic agent SN-38, has been observed (61,64). Studies determining the association of UGT1A1 alleles with estrogen metabolism and risk modification of breast cancer have not yet been reported, but they will be of great interest.
Estrogen Dominance
Too much estrogen (estrogen dominance) causes the body to become less sensitive to thyroid hormone. In other words, you will have normal or low thyroid hormone by lab test, but look hypothyroid. Thus, too much estrogen causes hypothyroid even though lab tests are normal. If you are hypothyroid due to estrogen dominance, then you will have fat on the hips and thinning hair.
Effects of Estrogen Dominance
1. When estrogen is not balanced by progesterone, it can produce weight gain, headaches, bad temper, chronic fatigue and loss of interest in sex - all of which are part of the clinically recognized premenstrual syndrome.
2. Not only has it been well established that estrogen dominance encourages the development of breast cancer thanks to estrogen's proliferative actions, it also stimulates breast tissue and can trigger fibrocystic breast disease - a condition which wanes when natural progesterone is introduced to balance the estrogen.
3. Excess estrogen implies a progesterone deficiency. This, in turn, leads to a decrease in the rate of new bone formation in a woman's body by the osteoblasts - the cells responsible for doing this job. Although most doctors are not yet aware of it, this is the prime cause of osteoporosis.
4. Estrogen dominance increases the risk of fibroids. One of the interesting facts about fibroids is that, regardless of the size, fibroids commonly atrophy once menopause arrives and a woman's ovaries are no longer making estrogen. Doctors who commonly use progesterone with their patients have discovered that giving a woman natural progesterone may cause fibroids to atrophy.
5. In estrogen-dominant menstruating women where progesterone is not peaking and falling in a normal way each month, the ordered shedding of the womb lining doesn't take place. Menstruation becomes irregular. This condition can usually be corrected by making lifestyle changes and using a natural progesterone product. It is easy to diagnose by having a doctor measure the level of progesterone in the blood at certain times of the month.
6. Endometrial cancer (cancer of the womb) develops only where there is estrogen dominance or unopposed estrogen. This, too, can be prevented by the use of natural progesterone. The use of the synthetic progestins may also help prevent it, which is why a growing number of doctors no longer give non-human estrogens without combining them with progesterone drug during HRT. However, all synthetic progestins have side effects.
7. Water logging of the cells and an increase in intercellular sodium, which predispose a woman to high blood pressure or hypertension, frequently occur with estrogen dominance. These can also be side effects of progestins use. A natural progesterone cream often resolves this problem.
8. The risk of stroke and heart disease is increased dramatically when a woman is estrogen-dominant.
2. Many peri- or post-menopausal women with clinical signs of hypothyroidism, such as fatigue, lack of energy, intolerance to cold, are actually suffering from unrecognized estrogen dominance and will benefit from supplementation with natural progesterone.
3. Estrogen and most of the synthetic progestins increase intracellular sodium and water uptake. The effect of this is hypertension.
4. Whereas estrogen impairs homeostatic control of glucose levels, natural progesterone stabilizes them. Thus, natural progesterone can be beneficial to both those with diabetes and those with reactive hypoglycemia. Estrogen should be contraindicated in patients with diabetes.
Progesterone increases sensitivity of estrogen receptors, and can therefore redirect estrogen activity and inhibit many of unopposed estrogen's undesirable side-effects, which includes interference with thyroid hormone activity.
Cold hands and feet, often caused by low thyroid function, may be a symptom of estrogen excess or low progesterone influencing thyroid function.
List of Estrogen Dominance Symptoms
Acceleration of aging
Agitation or Anxiety
Allergy (asthma, hives, rashes, sinus congestion)
Autoimmune disorders Lupus, Thyroiditis (Hashimoto's)
Breast cancer (men and women)
Breast tenderness with period
Cervical dysplasia (abnormal pap smear)
Cold hands and feet
Copper excess
Decreased sex drive
Depression with anxiety or agitation
Dry eyes
Fat gain around abdomen hips and thighs
Fibrocystic (lumpy breasts)
Foggy thinking
Gall bladder disease
Hair loss
Hypoglycemia (low blood sugar esp. 3-4 pm)
Increased blood clotting
Irregular menstrual periods
Magnesium deficiency
Memory loss
Mood swings
Ovarian cancer
Ovarian cysts
Polycystic ovaries
Pre-menopausal bone loss
Prostrate cancer (in men)
Sluggish metabolism
Thyroid dysfunction
Uterine cancer
Water retention, bloating
Zinc deficiency
Men produce estrogen (Estradiol) but in much lower amount than women. Men also produce progesterone, but about half the amount from that of females. Progesterone is made in men by the adrenal glands and testes. Progesterone is vital to good health in both women and men. It is the primary precursor of our adrenal cortical hormones and testosterone. The male hormone, testosterone, is an antagonist to estradiol (E2). It is made from progesterone. Men normally continue to produce relatively normal level of testosterone for their age and well into the seventies. Contrary to common perception, testosterone does not cause prostate cancer. Young men have high levels of testosterone and old men low levels. If testosterone were the cause of prostate cancer, young men would be dying of prostate cancer. Studies had shown that men with the highest level of testosterone have the least prostate enlargement. Conversely, men with the highest level of estrogen have enlarged prostates. Declining testosterone from aging, together with increasing level of estrogen, is the most likely reason for prostate enlargement and cancer in men.
The prostate is embryologically the same as the uterus in the female. Research Studies (Listed at the end of this newsletter) have shown that when prostate cells are exposed to estrogen, the cells proliferate and become cancerous. When progesterone or testosterone was added, cancer cell dies.
6 What are the symptoms of "estrogen dominance"?
According to John R. Lee, M.D.*, symptoms of estrogen dominance that men can experience include weight gain, bloating, mood swings, irritability, headaches, fatigue, depression and hypoglycemia. Estrogen dominance is known to contribute to cancer of prostate and the breast. It may seem paradoxical, but men are not immune to breast cancer.

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